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J Ethnopharmacol. Natural products from Cuscuta reflexa Roxb with antiproliferation activities in HCT colorectal cell lines. Nat Prod Res. Review on pharmceutical properties and conservation measures of Potentilla fulgens Wall ex Hoo-a medicinal endangered herb of higher Himalaya.

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Ahirwar RK. Diversity of ethnomedicinal plants in Boridand forest of district Korea, Chhattisgarh, India. Am J Plant Sci. Plant and Human Health. Volume 1. Springer, Cham: Ethnobotany of medicinal plants for livelihood and community health in deserts of Sindh-Pakistan; pp. Kala CP. Ethnomedicinal botany of the Apatani in the Eastern Himalayan region of India. Documentation of plant-based remedies of a folk herbalist of Comilla district, Bangladesh. Khatun MM, Rahma M.

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Determination of total phenolic, flavonoid, alkaloidal contents and in vitro screening for hepatoprotective activity of Cuscuta epithymum L whole plant against CCl4 induced liver damage animal model. Int J Pharm Pharm Sci. Medicinal plants used in Iranian traditional medicine to treat epilepsy. Higher plants-the sleeping giant of drug development. Phytochemicals: nutraceuticals and human health.

J Sci Food Agric. Ethnomedicinal demography and ecological diversification of some important weeds from district attock Pakistan. Pak J Weed Sci Res. Rapid densitometric method for simultaneous analysis of umbelliferone, psoralen, and eugenol in herbal raw materials using HPTLC. J Sep Sci. Qualitative and quantitative analysis of phytochemicals of Taraxacum officinale.

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Concordance between antioxidant activities and flavonol contents in different extracts and fractions of Cuscuta chinensis. Food Chem. Two new lignan glycosides from the seeds of Cuscuta chinensis. J Asian Nat Prod Res. Unusual ether-type resin glycoside dimers from the seeds of Cuscuta chinensis. Studies on the Chemical Constituents of Cuscuta chinensis. Ethnopharmacological investigations of phytochemical constituents isolated from the genus cuscuta.

Wink M, Witte L. Quinolizidine alkaloids in Genista acanthoclada and its holoparasite, Cuscuta palaestina. J Chem Ecol. J Pharm Biomed Anal. Cuscuta reflexa as a rich source of bioactive phenolic compounds. J Herbs Spices Med Plants. Isolation and characterization of bioactive metabolites in Cuscuta reflexa Roxb.

Swarnalin and cis-swarnalin, two new tetrahydrofuran derivatives with free radical scavenging activity, from the aerial parts of Cuscuta reflexa. A new flavanone, reflexin, from Cuscuta reflexa and its selective sensing of nitric oxide. Appl Biochem Biotechnol. Chemical characterization of the flavonoid constituents of Cuscuta reflexa. Awasthi LP. The purification and nature of an antiviral protein from Cuscuta reflexa plants. Arch Virol. Food Nutr Sci.

Zhan W, Zhisheng H. Studies on the chemical constituents of the seed of chinese dodder Cuscuta chinensis Chin Tradit Herb drugs. Characterization of phenolic compounds in the Chinese herbal drug Tu-Si-Zi by liquid chromatography coupled to electrospray ionization mass spectrometry. Rapid Commun Mass Spectrom. Lignan and flavonoid phytoestrogens from the seeds of Cuscuta chinensis. J Nat Prod. Components of the ether-insoluble resin glycoside fraction from the seed of Cuscuta australis.

Phytochemical study and evaluation of the antimicrobial activity and cytotoxicity of Cuscuta racemosa. Rev Bras Farm. Shailajan S, Joshi H. Cytotoxic cardiac glycoside from the parasitic plant Cuscuta reflexa. Elemental and fatty acid content of four medicinal plants: Kaiempferia rotunda, Cuscuta reflexa, Centella asiatica and Asparagus racemosus. European J Med Plants. Bais N, Kakkar A. Identification of bioactive constituents from different fractions of stems of Cuscuta reflexa Roxb.

Using GC-MS. Carotenoids of dodder Cuscuta reflexa grown on hedge, Clerodendrum enermy. Adv Nat Appl Sci. Studies on the chemical constituents of the herba of Cuscuta chinensis. J Chinese Med Mat. Fatty acid in the Cuscuta chinensis lam by capillary gas chromatography. Acad Periodical Farm Prod Process. Antioxidative constituents from the seeds of Cuscuta chinensis. Nat Prod Sci. Furofuran lignans from Cuscuta chinensis. Chin J Chem. Chemical constituents of the seeds of Cuscuta chinensis Lam.

J Shenyang Pharm Univ. Angiotensin converting enzyme inhibitors from Cuscuta japonica Choisy. Carotenoid pigments in the stem of Cuscuta australis. Hongzhu G, Jiashi L. Study on constituents of the seed from Cuscuta Australis. Guo H, Li J. Study on flavonoids of Cuscuta australis R.

China J Chin Materia Med. J Liq Chromatogr R T. Bacchi EM. Flavonoids from Cuscuta racemosa. Planta Medi. Chemical constituents and radical scavenging activity of Cuscuta pedicellata seed extracts. Int J ChemTech Res. Plant Physiol Biochem. Prior RL, Cao G. Antioxidant phytochemicals in fruits and vegetables: diet and health implications.

Hort Sci. Rice-Evans C. Flavonoids and isoflavones: absorption, metabolism, and bioactivity. Free Radic Biol Med. Applied Microbiology Microbial Biotechnology. Bioactive compounds content and their biological properties of acetone extract of Cuscuta reflexa Roxb. Evaluation of anticovulsant and anioxidant activity of selected medicinal plants. Nanoparticles formulation of Cuscuta chinensis prevents acetaminophen-induced hepatotoxicity in rats. Food Chem toxicol. Cuscuta chinensis seeds water extraction protecting murine osteoblastic MC3T3-E1 cells against tertiary butyl hydroperoxide induced injury.

The protective effect of flavonoids from Cuscuta chinensis in PC12 cells from damage induced by H2O2. J Chin Med Mater. Int J Pharm Clin Res. Hepatoprotective and antioxidant activity of ethanolic extract of aerial parts of Cuscuta reflexa Robx on liver damage due to cisplantin in rats.

Global estimates of the prevalence of diabetes for and Diabetes Res Clin Pract. Antidiabetic effects of Cuscuta reflexa Roxb in streptozotocin induced diabetic rats. Nat Prod Bioprospect. Effects of Cuscuta chinensis polysaccharide on diabetic mice by alloxan.

Anhui Med Pharm J. Aqueous extracts of Cuscuta chinensis Lam induces differentiat ion of amelanotic melanocytes of human hair follicles. Chin J Dermatovenereol. Protective effects of the Chinese herbal medicine prescription Zhujing pill on retina of streptozotocin-induced diabetic rats.

Biomed Pharmacother. Evaluated the Up—regulation in gene expression of hepatic insulin gene and hepatic insulin receptor gene in type 1 diabetic rats treated with Cuscuta chinesis Lam. J Babylon Univ. Trinchieri G.

Cancer and inflammation: an old intuition with rapidly evolving new concepts. Annu Rev Immunol. In vitro anti-inflammatory and anti-cancer activities of Cuscuta reflexa Roxb. Evaluation of carrageenan induced antiinflammatory activity of stem extracts of Cuscuta reflexa Roxb in rats. Int J Res Pharm Chem. Chin J Nat Med. Antinociceptive and anti-inflammatory activities of Cuscuta chinensis seeds in mice.

The Am J Chin Med. Evaluation of in vivo and in vitro biological activities of different extracts of Cuscuta arvensis. Nat Prod Commun. GC-MS analysis and antibacterial activity of Cuscuta reflexa against bacterial pathogens. Asian Pac J Trop Dis. Antibacterial activity of Cuscuta reflexa stem and Corchorus olitorius seed. In Vitro antimicrobial assessment of selected plant extracts from pakistan. Iran J Sci Technol A. An assessment of the antimicrobial properties of extracts of various polarities from Chasmanthera dependens, Emilia coccinea and Cuscuta australis, herbal medications for eye diseases.

J Appl Sci. Bonjar S. Evaluation of antibacterial properties of some medicinal plants used in iran. Study effect of plant extraction for Cuscuta europaea Dodder against two species of bacteria Staphylococcus aureus and Escherichia coli. J Contemp Med Sci. Effect of crude extracts and fractions of Cuscuta campestris and two different hosts on peripheral blood mononuclear cells and HIV replication. Int J Biosci. Molecular screening of chinese medicinal plants for progestogenic and anti-progestogenic activity.

J Biosci. Alaoui-Jamali M. Alternative and complementary therapies for cancer: Integrative approaches and discovery of conventional drugs. In vitro cytotoxic effects of Cuscuta chinensis whole extract on human acute lymphoblastic leukemia cell line. Iran J Med Sci. Faseb J. Equol: a comparison of the effects of the racemic compound with that of the purified S-enantiomer on the growth, invasion, and DNA integrity of breast and prostate cells in vitro.

Nutr Cancer. Phytochemical profiling and evaluation of the hepatoprotective effect of Cuscuta campestris by high-performance liquid chromatography with diode array detection. Anal Lett. Behbahani M. Evaluation of in vitro anticancer activity of Ocimum basilicum, Alhagi maurorum, Calendula officinalis and their parasite Cuscuta campestris. PloS one.

Adjuvant effect of ethanol extract of semen cuscutae on the immune responses to ovalbumin in mice. Kaempferol from semen cuscutae attenuates the immune function of dendritic cells. Comparative study on immune enhancement effects of four kinds of dodder seeds in shandong province.

J Chin Integr Med. Effects of alcohol extract from Polygonatum odoratum and Cuscuta australis on immunological function of mice injured by burns. Chin J Chin Mater Med. Study of Cuscuta australis hyperoside on immunological function of mice in vivo and in vitro. Effect of Cuscuta chinensis glycoside on the neuronal differentiation of rat pheochromocytoma PC12 cells. Int J Dev Neurosci. Effect of improving memory and inhibiting acetylcholinesterase activity by invigorating-qi and warming-yang recipe.

Effects of a polysaccharide from CCL on inhibiting oxygen free radical threshold of senile mice model. Acta Acad Med Mil Tertiae. Advances and challenges in screening traditional chinese anti-aging materia medica. In addition, it has been postulated that below certain HCHO concentrations ppm the mucous layer can trap and remove inhaled HCHO, thus preventing it from reaching underlying cells.

However, once the removal capacity of the mucous layer is exceeded, HCHO can then begin to affect the underlying cells as described in the section above. If the mucous layer removed inhaled HCHO below 1 ppm then it would represent a threshold phenomenon at least for the nasal cavity. However, the evidence for this is lacking and the idea is directly contradicted by experimental data.

The discussion below describes the effects caused by HCHO on the mucocilary system and the support for the "barrier" action postulated. The nasal cavity is primarily composed of ciliated respiratory and olfactory epithelium which is covered by a moving blanket of mucus.

The first function of the nose is to inform us of the presence of noxious gases, if these stimulate the receptors of the olfactory nerves. The second function of the nose is to drain the secretions of the sinuses and of the lacrinal tear glands. The third function of the nose is to prepare the inhaled air for the lungs. This includes warming, aoistenlng? Dust and many bacteria found in the inspired air are precipitated in the mucous that bathes the mucous membrane and, by the action of the cilia of the nasal passage, are moved outward Tuttle et al.

As research by Morgan et al. Using in vitro and in vivo techniques, Morgan et al. Results of the in vitro analysis indicate that mucus was present as a flowing continuous coat over the respiratory epithelium except on the most anteriorcentral extremity of the nasoturbinates and the anteriomedial extremity of the maxilloturbinates.

Mucous flow rates ranged from 0. At 15 ppm there was significant inhibition of mucociliary activity which progressed from anterior to posterior regions of nasal tissue. Only slight effects were noted in animals exposed to 2 or 6 ppm. Finally, using frog palate, Morgan et al. The above results indicate that a concentration relationship exists where mucociliary flow would be impaired at 15 ppm and less so at 6 and 2 ppm.

This range corresponds to the range where the steep dose-response in carcinogenicity of HCHO was seen in the Kern et al. Whether the mucous layer has some finite capacity to absorb HCHO and wash it away to prevent it from reaching the underlying cells, or the response seen is simply the overt signs of gradual cell toxicity, is unknown.

However, a number of factors must be considered when discussing the protective ability of the mucous layer. First, humans can detect HCHO at levels below 1 ppm which indicates that, at least in the olfactory region of the nasal cavity, HCHO is not completely removed by the mucous layer. The mucous layer is reported to be immobile or flowing extremely slowly in this region CUT, This was not.

The significant neoplastic and nonneoplastic effects were generally seen in the anterior regions of the rat nasal cavity. Second, in a study by Casanova-Schmitz et al. These data do not support the concept that at doses lower than ppm the mucous layer can act as a sink for inhaled HCHO which prevents it from reaching underlying cells. Finally, no data have been presented that show that HCHO is bound and removed by the mucous layer.

This is not to say that the raucous layer has no capacity for HCHO removal, but in the face of no pertinent data in this regard and the results of the Casanova-Schmitz et al. To what degree the mucous layer protects against HCHO's cytotoxic effects is not clear, but the experimental data do not suggest a large role for this.

Although it seems probable that some HCHO could react with protein in the mucous layer, data have not been developed to show that the ratio between the airborne concentration and the amount entering target cells is nonlinear, on the contrary, data have been developed to show that it is linear. Regarding the impact of changes in respiratory response to sensory irritants, it is likely that this response is responsible for the different response of rats and mice in the Kern et al.

Also, other data presented by Swenberg et al. Kern et al. Metabolism and Pharaacokineti. Absorption HCHO can enter the body as a result of inhalation, ingestion, or dermal absorption. Studies by Heck et al. In another study by Heck et al.

Measured HCHO concentrations were as follows; 0. Following oral exposure of dogs to HCHO, formate levels in the blood increased rapidly, indicating rapid uptake and metabolism Malorny et al. Dermal absorption has been demonstrated in guinea pigs Usdin and Arnold, , but does not appear to be significant in comparison to inhalation or ingestion. The chemical form of the radiolabel has not been determined, but it has been reported by Ulsamer et al.

Pharroacokinetics 4. The conversion of HCHO to formate occurs following intravenous i. Studies using i. This becomes undetectable within 1 hour after cessation of infusion. The peak formate concentration following HCHO infusion was the same as when formate 0. The plasma half-life for formate between 80 and 90 min. Similar experiments using Cynomolgus monkeys, in which 0.

Similar half-lives for blood HCHO have been observed in rats, guinea pigs? Studies by Heck b have shown that C] formate and C] HCHO have similar distribution patterns in rat blood cells and plasma following i. In a somewhat different experiment, McMartin et al. Again, HCHO could not be detected in the blood although formate levels increased rapidly. A study in which humans were exposed to HCHO gas 0. In a more recent study by Heck et al.

The rats 8 exposed and 8 controls were exposed to approximately No significant differences were seen between exposed and control rats. Six human volunteers 4M, 2F were exposed to 1. Venous blood was analyzed for HCHO levels before and after exposure. However, significant differences were seen in some of the subjects' either decrease or increase HCHO concentration between blood taken before and after exposure.

The rapid conversion of HCHO to formate occurred in many tissues in the various species examined, including human. The enzymes involved have been studied by Strittmatter and Ball as well by Uotila and Koivusalo The oxidative process is initiated by formation of S-formyl glutathione, which is then oxidized by NAD and finally cleaved by thiol esterase, releasing formic acid and glutathione.

HCHO also has been reported to be oxidized to formic acid by a nonspecific aldehydehydrogenase and through the tetrahydrofolic acid pathway Huennekens and Osborn, Neely administered radiolabelled HCHO intraperitoneally i. At lower doses, only radiolabelled methionine. The author postulated that CO2 was derived from serine formed from glycine and N5,N10 methylene tetrahydrofolate by deamination to pyruvate and oxidation in the Krebs cycle.

In a study by Mashford et al. Formation of roethionine would also account for the labelled choline observed by Duvigneaud et al. More recent work by Pruett et al; has demonstrated the incorporation of 14C-HCHO into the nucleic acid and protein fractions of in 38 human diploid fibroblasts. Casanova-Schmitz et al.

In addition to the serine pathway to C02 postulated above Neely, , two other pathways have been identified, and are diagrammed in Figure Reactions are: la, HCHO dehydrogenase GSH ; Ib, aldehyde dehydrogenase; Ic, catalase peroxidatic mode ; 2a, formyltetrahydrofolate synthetase; 2b, forroyltetrahydrofolate dehydrogenase; 2c, catalase peroxidatic mode.

This has been demonstrated in rat liver perfusates Waydhas et al. Tetrahydrofolic acid pathway and 1-carbon transfer for HCHO metabolism. Oxidative demethylation of N,N-dimethylglycine from choline degradation also contributes significantly to endogenous HCHO. The rate of HCHO oxidation to formate exceeded the rate of HCHO production in perfused rat liver by a factor of 12 when aminopyrine was used as the substrate for the demethylation reaction.

Whereas the conversion of HCHO to CO2 occurs in a similar manner in the different, species studied, the relative importance of each reaction differs among species and tissues. Thus, the rat is able to convert formate to CO2 at more than twice the rate of monkeys or humans and, as a result, has lower blood formate levels McMartin et al.

Summary In summary, free HCHO is not usually found in plasma or other body tissues in measurable quantities, endogenous HCHO that is produced may be reasonably presumed to be metabolized rapidly to formate or to enter the one-carbon pool. The same pathways seem to occur in all mammalian species examined to date, but reaction rates differ among various species and tissues. Neither the ratio of metabolic deactivation to binding to tissue or small molecules nor the effect of route of exposure on this ratio is known at this tine.

Thus, although Egle's work suggests that the respiratory tract tissues would receive the greatest dose, other body sites cannot be ruled out. The possibility exists, that the actual carcinogenic agent may be an amino acid or other adduct EPA, Structure-Activity Relationships HCHO is structurally similar to other aldehydes such as acetaldehyde, malondialdehyde and glycidaldehyde. These aldehydes have been shown to have oncogenic activity in laboratory animals. For instance, inhalation of acetaldehyde has produced tumors of the nose and larynx in hamsters and tumors of the nose in rats, when administered by inhalation, and glycidaldehyde has produced skin tumors in mice in skin painting tests.

Since acetaldehyde is the closest in structure to HCHO, and its effects on animals have been compared in a previous section, the significant studies related to its oncogenic potential will be described. It had weak mutagenic activity in the fruit fly Drosophila melanogaster Rapoport, The potential of acetaldehyde to damage chromosomes has been indicated by the dose-dependent sister chromatid exchanges in the Chinese hamster ovary cells Obe and Ristow, and human lymphocyte cells Ristow and Obe, The weekly concentrations of BP used were 0.

Control animals were exposed to air alone or simultaneously with the same concentrations of BP. At the end of the treatment period, 5 randomly selected animals from each group were killed and autopsied. All remaining animals were allowed to recover for 20 weeks and sacrificed by week Exposure of hamsters to ppm acetaldehyde vapor produced abnormalities in the respiratory tract which were characterized primarily by reversible hyperplastic, metaplastic, and inflammatory changes.

Neoplastic alterations attributable to acetaldehyde exposure alone were not found. However, such a synergistic effect of acetaldehyde was not noticeable at any of the lower BP levels. No significant differences in the number of tumors in the larynx, bronchi, bronchioles, or alveoli were found among the different treatment groups.

All remaining animals were sacrificed after weeks. Intratracheal administration of acetaldehyde at both dose levels caused severe hyperplastic and inflammatory changes in the bronchioalveolar region of the respiratory tract; however, only one case of pulmonary adenoma was found out of animals treated with acetaldehyde alone. This is not considered to be an indication of carcinogenic activity of acetaldehyde.

Despite the high degree and frequency of peribronchiolar adenomatoid lesions found following intratracheal instillation of acetaldehyde, the neoplastic response of the bronchioalveolar tissues was clearly lower in animals treated with BP plus acetaldehyde than in those given BP alone. Thus, acetaldehyde did not influence the carcinogenic effect of BP. Similarly, the carcinogenic effect of DEN was also not influenced by the treatment with acetaldehyde. In another study, Feron et al.

At the end of the exposure period week 52 , 3 animals per sex were taken from groups 1 and 2 for autopsy. All remaining animals were sacrificed after 81 weeks. At the end of the exposure period, i. No tumors were found in hamsters killed immediately at the end of the exposure period. Acetaldehyde-exposed animals which were found dead or sacrificed at week til exhibited inflammatory, hyperplastic, and metaplastic changes in the nose and larynx, suggesting a persistence of those alterations.

Tumors were encountered in the nose adenoma, adenocarcinoma, anaplastic carcinoma and the larynx papilloma, carcinoma in situ, squamous cell carcinoma, adeno-squanous carcinoma ; animals exposed to acetaldehyde plus BP or DEN also exhibited tumors of the trachea and the lung.

The neoplastic and nonneoplastic lesions in the larynx were mainly located either on the true vocal folds or in the most anterior part of the larynx. None of the animals exposed to air alone demonstrated nasal or laryngeal tumors nor atypical laryngeal hyperplasia and metaplasia. Carcinomas in situ and squamous cell carcinomas of the larynyes were found after combined treatment, but were not observed after treatment with either BP or DEN alone.

Finally, in a study by Woulersen et al. There was significant nonneoplastic lesions of the olfactory epithelium at each exposure level. In contrast, significant nonneoplastic lesions were seen in the respiratory epithelium only at the highest dose- Statistically significant numbers of adenocarcinomas were observed at each dose level in males and females.

Squamous cell carcinomas were observed at the two highest dose levels in males and at the highest dose level in females. Most of the tumors originated from the olfactory epithelium. Table presents summary tumor response of the nasal cavity for this study. Figures in brackets represent the number of animals from which this tissue was examined microscopically. In this table, a benign tumor is ignored if a malignant tumor of the same histogenetic origin is also present in the same tissues.

The new studies released since have broadened our knowledge regarding the potential carcinoyenicity of HCHO. The new epidemiologic studies have contributed stronger evidence and have supported previous studies which suggested HCHO may be a human carcinogen. In particular, the Epidemiology Panel of the Consensus Workshop on Formaldehyde and the EPA b examined a group of studies and concluded that a group of professionals anatomists, patholoyists, embalmers, and undertakers have a significantly increased mortality from leukemias and brain neoplasms.

These excesses in mortality can not be attributed to diagnostic bias since these excesses remained when other professional or like socioeconomic groups were used as referents Consensus Workshop on Formaldehyde, In addition, epidemiologic information in the form of one study and one abstract report increased nasal cancer risks with HCHO exposure.

Although all the studies are of cohort or case-control design, designs essential for judging causality, many of the studies suffer from limitations that influence their conclusions. Major drawbacks are: 1 the inability to separate the contributions of HCHO from the contributions of other occupational or personal exposures; 2 small sample sizes for the cohort studies; 3 insufficient follow-up; and 4 low statistical power.

The following text describes the current pool of epidemiologic data with study designs and findings highlighted. Table identifies these studies. Tables through present selected power calculations for several of the studies shown in Table These studies are either cohort or case-control designed.

If a study is likely to claim that the exposure is not associated with a disease, when in fact an association existed, it has a low power for detecting that association. An SMR divided by is called a risk ratio. If the disease under study is rare, the odds ratio is numerically very close to its associated SMR, but the causal inference is not as direct. In addition, an odds ratio obtained from a case- control study nested within a cohort design can be used to support conclusions from the cohort study.

Tirladai only tajrkan with 2. J9R4 nasal cancer cases in Denmark Hayes et al. Obtained from the studv by Faverweather ot al. Ten studies are of chemical or industrial workers and seven studies of medically-related professions. The medically- related professions represent formalin exposures such as those encountered by morticians, embalmers, anatomists, and pathologists..

This group has other chemical exposures, but by nature of their professions, formalin is an integral component and represents the exposure of concern. Lastly, six other case- control studies examine an occupational etiology of nasal cavity and sinus cancers. These studies examine the relationship between nasal cavity and sinus cancer and HCHO exposure or between these cancers and particular occupational groups where HCHO has been known to occur.

Matanoski of John Hopkins University examined mortality patterns of male pathologists in two professional societies. When compared to U. Matanoski continued following this cohort until and reported a 3-fold significant excess of lymphatic and multiple myeloma tumors and a 2-fold excess of brain cancers when compared to age-specific rates for U. Combining the two groups without overlap, about individuals, Matanoski reported increased mortality from lymphatic 3-fold excess, pjCO.

In the period, deaths occurred. Stroup et al. No increasing risks were observed with increasing years of exposure. Tabershaw Associates did not use an unexposed group as a comparison, but compared the exposed employees to those with less than 5 years of exposure. Friedlander et al. These workers had been exposed to HCHO, along with other photographic chemicals. In the mortality study, Friedlander et al. From the incidence analysis, Friedlander et al.

The use of a local comparison may have overestimated the number of expected lung cancer deaths. In a subsequent analysis of the mortality data for lung cancer among individuals employed at this plant, Acheson et al. Marsh of the University of Pittsburgh conducted an SMR analysis and a case-control study nested within the cohort of a Monsanto chemical plant. This plant produced plastics and workers had potential exposures to HCHO, vinyl chloride, styrene, and cellulose acetate.

Marsh compared the mortality experience of all workers to the white male populations of the U. In the SMR study, the cohort consisted of 2, male workers with a minimum of one year employment. Among the 2, workers, deaths were identified by the company or by death certificate searches. Fayerweather et al. Thus, these analyses were performed on an incomplete cohort and the results may be biased.

Brinton et al. None of the increased odds ratios was significant in the presence of control for confounding variables. This ratio was unstable, based on only one male and one female. The industries included textile and cotton mills, apparel manufacturing, and hosiery.

When histologic types of nasal cancer were evaluated, both males and females were found to be at increased risk of nasal adenocarcinoma, with further enhancement of risks for those experiencing dusty work conditions. The authors stated that this study provides further evidence of an association between employment in the textile industry and risk of nasal cancer.

Tola et al. Forty-five cases were collected from the Finnish Cancer Registry between and and were aye-sex matched to non- respiratory cancer controls. Other factors significantly associated with the cases were histories of serious nasal trauma, chronic rhinitis, and sinusitis. Smoking was not significantly associated with nasal cavity and sinus cancer.

Hernberg et al. One hundred seventy cases diagnosed between and and reported to the prospective cancer registries were selected. Each case was sex-country-age at diagnosis matched with colorectal cancer controls. Stayner et al. In this cohort, which represented three plants in two different states, Stayner et al. Walrath and Fraumeni of NCI conducted a py. R study of 1, funeral directors or embalmers licensed in New York. Marsh found death among male workers with exposure of one month or greater in a "formaldehyde related plant area".

Marsh compared their mortality experience to U. To adjust for the healthy worker effect, age, sex, and race-standardized PCMRs based on county comparisons were also calculated. Race-age-sex adjusted PMRs were significantly elevated for cancer of the colon based on U. Liebling et al. Furthermore, the authors postulated that besides nasopharyngeal cancer, an association between HCHO exposure and cancer of the buccal cavity and pharynx in humans is biologically feasible since humans breathe through both the nose and nouth, while rats and mice are obligatory nose-breathers.

Like many "other studies, this study is limited by the inability to completely separate HCHO exposure from exposure to other chemicals. Olsen et al. The researchers used a nationwide data linkage system which has linked cancer cases and previous employment. Occupational histories came from the National Supplementary Pension fund, established in , and the Central Population Registry.

Use of these national data sets eliminated tne potential for recall bias since cases and controls were not interviewed. In this case-control study, Olsen et al. In this analysis, the elevated risk with HCHO exposure was reduced to 1. The Hayes et al. Living and deceased population controls were used as the comparison group, but Hayes et al.

Hayes et al. In addition, Hayes et al. Bertazzi et al. The mortality experience of 1, male employees who had worked six 6 months or more between and was compared to the expected number of deaths using national and local rates. For the entire cohort, Bertazzi et al.

Mortality from digestive neoplasms and lymphopoeitic neoplasms was nonsignificantly elevated. In this analysis, the increased mortality from lymphatic and hematopoietic system and from digestive neoplasms was observed only among the HCHO exposed. Elevated mortality was observed in both the HCHO exposed and nonexposed groups. Delzell and Grufferman of Duke University examined the mortality experience of 4, deaths between of white female textile workes.

Deaths and occupation as recorded on the death certificates were identified from state computer files. In this study, textile worker occupational code included workers in industries that manufactured textile mill products, apparel, or other fabricated textile products. Delzell et al. The elevated mortality from all lymphopoietic sites and from specific lymphopoietic sites are particularly interesting since HCHO, along with other chemicals, may comprise exposures in textile mills.

EPA used an exposure level of 0. Since this study was unable to identify individual exposures, we do not know if any or all deaths may have had previous HCHO exposure. Conclusion The epidemiologic literature report, for the first time, a significant association between nasal cancer and HCHO. This observation was confounded due to wood dust exposures, but when the analyses controlled for wood dust, the risk remained elevated nonsignificantly. A critical review of the Hayes et al.

These observed excesses can not be explained by diagnostic bias or socioeconomic factors. Low power is a characteristic of several studies Tables through Selecting lymphatic and hematopoietic cancer as an example, Table shows that Levine et al. Insufficient follow-up and small sample sizes contribute doubly to low power through insufficient person-years and through cancers not yet having appeared. Thus, absence of significant elevations in either brain cancer, lymphopoietic cancer, or leukemia in individual studies should not override the findings in Matanoski, Stroup et al.

Secondly, the discussed studies lack historical exposure estimates and this cannot resolve the possible contributions of HCHO from other chemicals. Leukemias and brain cancers have been associated with other occupational groups. These occupational groups are exposed to solvents, benzene, and other organic chemicals.

These exposures may be like those of the medically-related professions and the chemical manufacturing workers. Additionally, through case-control methods, an association between nasal cancer and HCHO has been observed in one study and a suspect association has been reported in an abstract of another study. At this time, there is limited evidence that HCHO may be a human carcinogen. Assessment of Human Evidence EPA has determined, based upon its proposed cancer risk assessment guidelines, that there is limited evidence that HCHO may be a human carcinogen.

As discussed in the Epidemiology section, the literature reports Hayes et al. However, these observations were confounded due to wood dust exposures. When the analyses controlled for wood dust, the risk remained numerically elevated but lost its statistical significant pO. These observed excesses cannot be explained by diagnostic bias or socioeconomic factors. The determination that there is limited human evidence is based on an examination of the technical merits power, follow-up, confounding, etc.

In the CUT study, statistically significant numbers of squamous cell carcinomas of the nasal cavity of Fischer male and female rats were seen. The CUT study was a well conducted, multidose inhalation study. In addition, while not statistically significant, a small number of squamous cell carcinomas were seen in male mice.

Because this type of nasal lesion is rare in mice, these data must be considered biologically significant. Supporting the findings above, are the results of the Albert et al. Additional support is provided by studies by Dalbey et al. HCHO is omtayenic in numerous test systems, and it is able to transform a number of cell lines. Its ability to interfere with DNA repair mechanisms has also been demonstrated. The literature reports conflicting data concerning chromosomal effects in humans.

However, the weight of this data indicates little if any potential for these effects in the workplace, but this judgement must be tempered by the limitations of the studies. Although HCHO's acute effects do not demonstrate its carcinogenicity, they do help explain differences in species response, and the severity of the carcinogenic response in the animal studies, HCHO's acute effects may be factor in the promotion of its carcinogenic potential at concentrations greater than 1 ppm in rats and possibly in humans.

Acetaldehyde, the closest aldehyde to HCHO in structure, is carcinogenic in hamsters and rats, causing cancers in the nose and trachea of the former, and nasal cancers in the latter, in addition, other aldehydes such as glycidaldehyde and malondialdehyde have been shown to be carcinogenic. Although the data indicate that HCHO is rapidly metabolized in in vivo and in vitro studies, and that transport to sites distant from the point of contact is unlikely, the fact remains that HCHO-DNA interaction is indicated for exposures below 2 ppm.

In addition, the finding of benign tumors in the Kern et al study at 2 ppm is consistent with a conclusion that HCHO is not metabolized removed before it can interact with nuclear material. The assumption is that there is a dose-response below 2 ppm for benign tumors and not a threshold just below 2 ppm.

Whether this pattern of interaction with DNA is linear or non-linear has not been unequivocally determined. In addition, it is impossible to say at this time, if ever, what level of rapidity of riCHO metabolism versus increases in exposure is an indicator of a threshold.

The defensive role of the mucous layer in preventing exposure of target cells to HCHO has been extensively discussed. In fact, the data indicate that a constant proportion of HCHO reaches the underlying cells. While this does not imply that the mucous layer offers no protection, it does not support a threshold hypothesis. The effect of sensory irritants on the respiratory rates of some laboratory animals is well known.

Such a response apparently contributes to the minimal neoplastic response seen in mice. This is an important factor when interpreting inhalation studies and in determining the dose actually received. While a reduction in respiratory rate protects the animal by reducing the amount of the irritant irihaled, J.

However, it is a factor in the generation of risk estimates since the nominal dose levels used for statistical purposes may need to be changed to reflect this effect. HCHO have Deen studied in rats, mice, hamsters, and monkeys by inhalation. In rats a highly statistically significant response was obtained in two strains.

In mice only males of one strain showed a marginal response, while hamsters and monkeys showed no neoplastic response. While mice did not show a statistically significant response, the response was biologically significant given the rarity of nasal tumors in mice. However, the studies of respiratory response to sensory irritants indicate that when dose received is adjusted for reductions in respiratory rate, rats and mice appear to respond similarly.

The cancer test data on hamsters are negative. However, the possibility exists that they may be responding to a sensory irritant in the same manner as mice. The study using monkeys indicates that, at least for nonneoplastic lesions squamous metaplasia , rats and monkeys respond similarly.

In addition, as a matter of policy EPA chooses to use the most sensitive species to predict human risk. Even though studies on the hamster show no observed tumors, the studies do not negate the rat data and there are no data to show that the hamster's response to HCHO exposure is more representative of the human response than is the rat's.

EPA's position is supported by the Risk Assessment Panel of the Workshop , which stated that there are "no indications that the response by humans would be different than that exhibited by rats, mainly due to the lack of experimental data pertaining to this issue. Qualitatively, the metabolic pathways of HCHO in rats and humans are similar. Again, no information exists demonstrating that the response would be quantitatively different as a result of differences in distribution of the inhaled dose.

Categorization of Overall Evidence In conducting risk assessments of suspect carcinogens, EPA generally evaluates the overall weight-of-evidence including both primary and secondary evidence of carcinogenicity.

In the process of categorizing HCHO, two lines of evidence were assessed, one of which is an assessment of studies of humans and the other is the assessment of evidence from studies in animals. The results from each assessment are then combined to characterize the overall evidence of carcinoyenicity. Consequently, based on the determination that there is sufficient evidence that HCHO is an animal carcinogen and the determination that there is limited human evidence, HCHO can be classified under the draft guidelines as a Group Bl-Probable Human Carcinogen.

At concentrations below 0. Eye irritation has been reported at concentrations as low as 0. At concentrations at or above 1 ppro, nose, throat, and bronchial irritation have been noted. Such irritation was nearly uniformly reported by persons when the concentration reached 5 ppra, ECHO concentrations exceeding 50 ppm cause severe pulmonary reactions, including pneumonia, bronchial inflammation, pulmonary edema, and sometimes result in death.

Table shows the variability and overlap of thresholds for responses among subjects. Although the severity of an effect in a person increases with increasing concentration and duration of exposure, a dose-response for an individual, the thresholds for the effects vary in the population as Table illustrates? The problem is to determine population dose- response relationships. Tolerance to olfactory, ocular, or upper respiratory tract irritation occurs in some persons.

Factors such as smoking habits, socioeconomic status, preexisting disease, and interactions with other pollutants and aerosols are expected to modify these responses. Some persons can detect HCHO at 0. Increased Dlink rates are noted at concentrations of 0.

Blink rate, although used as an objective measure of eye irritation, appears variable for any given subject. The irritant effects of HCHO seem to be accentuated when it is mixed with other gases. Accidental splash exposures of human eyes to aqueous solutions of HCHO have resulted in a wide variety of injuries, depending on concentration and treatment.

These range from discomfort and minor, transient injury to delayed, but permanent, corneal opacity and loss of vision. In summary, human eyes are very sensitive to HCHO, detecting atmospheric concentrations of 0. Tolerance to eye irritation is reported to occur. Lacrimation is produced at 20 ppm, but damage is prevented by closing the eyes in response to discomfort. Aqueous solutions of HCHO accidentally splashed into the eyes must be immediately flushed with water to prevent serious injury, such as lid and conjunctival edema, corneal opacity, and loss of vision.

Upper Airway Irritation Nose and Throat Symptoms of upper airway irritation include the feeling of a dry or sore throat, tingling sensation of the nose, and are usually associated with secretion of tears and pain in the eyes. Irritation occurs over a.

Tolerance to eye and upper airway irritation may occur after hours of exposure. However, even if tolerance develops, the irritation symptoms can return after a 1- to 2-hour interruption of exposure. Finally, examinations of the nose and throat reveal chronic changes that are more severe in persons exposed to the higher concentrations HCHO. Exposure to HCHO can cause alterations in the nasal defense mechanisms'kthat include a' decrease in -'.

Plyraonary edema and pneunonitis could result from very high HCHO concentrations, ppm. Astnma HCHO has been shown to cause bronchial asthmalike symptoms in humans. Persons with bronchial asthma respond to numerous agents, such as exogenous irritants and allergens, respiratory infections, cold air, smoke, dust, and stress. The asthmatic person seems to represent an extreme on the scale of respiratory sensitivity to inhaled irritants.

Diagnosis of immune sensitization has been based upon knowledge that individuals were exposed to HCHO before onset of symptoms, and on disease symptoms and the spirometric pattern of changes in respiratory function upon bronchial provocation by inhalation challenge with HCHO.

Although the production of specific Immunoglobulin Type E IgE antibody has been demonstrated to other chemicals e. Furthermore, respiratory aensitization with HCHO has not been demonstrated with animals this nay not be critical because there is not a veil recognized model for "asthma" nor in some human studies in which patients who complained of respiratory illness did not respond positively to bronchial challenge testing with HCHO gas.

Studies are underway to answer some of these points. Thresholds have not been established for the irritant effects of inhaled HCHO. However, within the range of 0. In most healthy persons exposed to HCHO, concentrations greater than 5 ppm will cause cough and possibly a feeling of chest tightness. In some susceptible persons, concentrations below 5 ppm can cause these symptoms, including wheezing.

In persons with bronchial asthma, the irritation caused by HCHO may precipitate an acute asthmatic attack, possibly at concentrations below 5 ppm. Sufficiently well- controlled studies are not available to definitively establish the development of respiratory tract allergy to HCHO as a gas.

In concentrations greater than 50 ppm, severe lower respiratory tract effects can occur, with involvement not only of the airways tout also of alveolar tissue. Acute injury of this type includes pneumonia and pulmonary edema. Irritation is a purely local, immediate response resulting from a chemical reaction between HCHO and the epithelial lining of the airways. The irritant response will resolve with cessation of exposure.

It is scientifically accepted that there is a threshold for the irritant response. A chemical sensitization response is a far more complicated physiologic effect. Some chemical sensitization responses are mediated by the immunologic system, for others antibodies have not yet been identified and the mechanism is as yet unknown.

The response is similar to an asthmatic reaction, it will not immediately resolve itself upon cessation of exposure and may require medical treatment. There is debate in -the scientific community as to whether or not a threshold exists for the initial chemical sensitizing event s , but the data is not available to resolve the issue. It is also probably a cause of immunologic contact urticaria Consensus Workshop, Besides contact with HCHO itself, allergic contact dermatitis can be caused by contact with disinfectants and tissue preservatives containing HCHO, HCHO releasers resins in clothing, and paper products , and with preservatives used for cosmetics, detergents, polishes, etc.

Table illustrates some induction concentrations which induce sensitivity and the range of challenge concentrations which elicit the allergic reaction. However, because of the i limited data base these estimates should be used with caution Consensus Workshop, Data induction and challenge concentrations regarding the ability of HCHO-resin treated textiles to cause contact dermatitis in garment workers for instance are lacking.

However, proof that the immunological reactions are due to an allergic response must await the demonstration of specific immune reactions such as the production of IgE or igG antibody specific for HCHO IRMC Subgroup on Sensitization, a. Nonimmunologic contact urticaria which requires multiple applications at the aame site has. Frequent eosinopnilia increase in eosinophil leukocytes and some severe hypersensitivity and asthma-like reactions have been associated with this occurrence.

The asthma- like reactions are suggestion of Type I allergy Consensus Uorkshop, Cellular Changes Inhalation exposure to HCHO causes a number of cellular effects depending on the concentration and duration of exposure. In a more recent study by Tobe et al. However, the frequency of squamous metaplasia falls within the 15 percent background rate for this type of lesion as seen in the Kern et al.

Table clearly shows that a threshold for this response exists at about 1 ppm rats in the Kern study experienced squamous metaplasia at 2. A similar threshold level is suggested for monkeys as Table indicates. Although, the authors did not attribute the one case of squamous metaplasia to HCHO exposure, it is possible that HCHO is causing effects at or below 1.

Such a response may be due to damaged cilia of the respiratory epithelium. Recently submitted data by Woutersen et al. Thus, monkeys and humans may be more sensitive to the effects of HCHO than rats nasal discharge was not observed in rats. Male Fischer rats were exposed for 6 hours per day for 1, 2, 4 or 9 days, to 0. There was a clear dose-dependent affect on mucociliary activity. Whether ultrastructural changes to cilia occurred below 2. Based on data developed in rats and monkeys the NOEL for squamous metaplasia and rhinitis can be placed at 1.

Ultrastructural changes in the mucocillary clearance system may be occurring as low as 0. The practical consequence of the cellular changes noted is a disturbance of the snucoeiliary clearance saeehanism. Central Nervous System Effects Reports in the literature link HCHO with a number of behavioral and physiologic effects such as thirst, dizziness and apathy, inability to concentrate, sleep disturbances, etc. Central nervous system responses to HCHO have been tested in a variety of ways, including by determination of optical chronaxy, electroencephalographically, and by measuring the sensitivity of the dark-adapted eye to light.

Responses are reported to begin in some persons at 0. HCHO at less than 0. Neurochemical Changes Studies using radio labeled HCHO have shown radioactivity in the brains of rats after inhalation exposures. However, the chemical identity of the radioactive material has not been determined. HCHO has been shown to affect the firing rate of nasopalatine and ethmoidal nerves of the trigeminal nasal sensory system.

Besides being able to effect changes in the respiratory rate of animals, HCHO also appears to be able to depress trigeminal nerve response to other irritants, although the data in this regard are not conclusive. In two studies reviewed by the Consensus Workshop 19B4 , conflicting results were seen. In contrast, monkeys injected intravenously over several hours with HCHO for a total dose of 0. Unfortunately, these studies for the most part have involved field surveys using subjective self-report symptom inventories.

This is a significant problem when dealing with HCHO, which in addition to any direct toxic effects possibly associated with it, produces distinct olfactory cues which may stimulate a spectrum of secondary psychological reactions e. Nine studies of human populations were reviewed by the Consensus Workshop , but most had serious methodologic problems.

For instance in studies by Dally et al. However, these studies do not include control populations and suffered from selection bias. Thun and Altman have pointed out some of the difficulties in prevalence surveys of symptoms in residents from UFFI homes, including olfactory cues, respondent and recall biases, and the objective outcomes measured.

No significant difference was found in the occurrence of headaches or insomnia in residents of homes with UPPI, compared to neighborhood controls. In contrast, a study by Olson and Dossing found a significantly greater prevalence of nose and throat irritation, unnatural tiredness, and headaches in exposed subjects than in controls. While this study overcomes many of the design problems previously discussed, responses still may have been based by an awareness of the subjects of the study goals and hypotheses.

A study by Schenker et al. In addition, a study by Anderson found no effect on performance tests of 16 healthy volunteers exposed to HCHO under controlled laboratory conditions Consensus Workshop. A more recent study by Kilburn et al. Various possibilities exist whereby such effects might be mediated.

Some evidence exists that exposure to formic acid the principal metabolite of formaldehyde in vapor form at high concentrations exercises nervous system toxicity in intact rats. The irritant effects of formaldehyde may be reflected in altered function of sensory nerves such as the trigeminal nasal sensory system.

The presence of morphological changes in the CNS has been observed in one study and not in another. Epidemiologic studies evaluating neuro- psychological symptoms potentially due to occupational or environmental exposure to formaldehyde have failed to overcome the problems commonly associated with such studies. However, some studies merit further investigation.

OavclopBental and Reproductive Effects 5. Animal Studies A number of studies have been reported which measured the potential of teratogenic or reproductive effects of HCHO. No teratogenic effects were reported. However, other effects in dams and fetuses were reported. A dermal study by Overman, as reviewed by Ulsamer et al. A repeat of the study did not bear this out. A study by Marks et al.

At the highest dose, 22 of the 34 pregnant mice died. At that dose, there was an increased incidence of resorptions, but that increase was not statistically significant. At no dose did the incidence of resorptions differ between the treated and control groups. There were also no treatment-related differences in the mean number of implantations, stunted fetuses, live fetuses per litter, or average fetal body weight per litter.

At a dose which killed more than 50 percent of the dams, no adverse reproductive outcomes were observed except for the increase in the incidence of resorptions that was not statistically significant. To measure the teratogenic potential of HCHO generated in vivo, a number of investigators exposed animals to hexamethylene- tetramine by feeding or by drinking water. Studies by Delia Porta et al. No malformations were noted in any of the studies. Ovarian involution and endomentrial atrophy were observed in another study, but only in female nice exposed to 40 ppm HCHO a concentration which killed 80 percent of the animals.

Other studies were reviewed but were found to be of little value because of gaethodologie problems. However, the Consensus Conference Panel stated that: There is indirect evidence that would argue against formaldehyde being a major human teratogen.

Over the last 30 years, the annual production and domestic use of formaldehyde in the United States has gone up fivefold from one billion pounds. Birth defects have been reasonably stable over the last 30 years, although in the last decade, there have been some exceptions to this rule.

The reported incidence of ventricular fteptal defects and patent ductus arterious has increased and that of anencephaly and spina bifida has declined. In addition, 30 percent of the exposed group had a history of menstrual irregularity. The Consensus Workshop felt that these two studies point to the need for further research, but do not show a cause-and-effeet relationship between exposure to HCHO and menstrual disorders.

In two other reports reviewed by the IRMC , an increased incidence of miscarriages, changes in menstrual cycles, and an increase in ovarian cysts were reported in one study of female histotechnicians while a high incidence of sexual dysfunction among male workers making fiber-reinforced plastic was reported in another.

In both instances, the workers were exposed to chemicals other than HCHO, especially the male workers, and the results may be due to the complex effects of numerous chemicals, rather than HCHO alone. NO evidence of increased dominant lethal effects were seen in a study by Epsteion et al. However, these data may not be inconsistent given different routes of exposure. More work in this area may be needed.

Commenting on the possibility of one type of germ-cell nutation the Workshop stated that "Human germ-cell mutations causing nondisjunction could result in an increase in Down's Syndrome. The constancy of maternal age-specific rates of Down's Syndrome over the last 30 years, in face of increased exposure, suggests that exposure to formaldehyde is not causing nondisjunction in humans. Conclusion Ulsamer et al. Also, the in vitro data do not provide any evidence to support the conclusion that formaldehyde causes terata at exposure concentrations that are not toxic to the adult.

Inhalation of formaldehyde has caused fetotoxic effects but not teratogenic effects. Further studies of formaldehyde exposure by inhalation are needed to elucidate the Meaning of these changes. Limited evidence suggests that formaldehyde may affect the Menstrual cycle and perhaps reproduction in women repeatedly exposed. Additional work is needed to validate these findings. XRMC Subgroup: Reproductive function depends upon a sensitive and integrated feedback system between the nervous system and the reproductive organs.

Thus, many chemicals that affect the nervous system have the potential to affect reproduction. It is possible that formaldehyde, by affecting the nervous system induces indirect changes in reproductive behavior and reproduction. Consensus Panel: In summary, the panel could find no evidence clearly demonstrating that formaldehyde caused adverse reproductive outcomes.

What it found was a paucity of information from which to make inferences and data that suggested hypotheses to be tested in future studies. This panel feels that formaldehyde poses little, if any, risk as a potential human teratogen. This judgment is based on the irritation potential of formaldehyde at extremely low ambient concentrations 0. One recent review article by Beall et al.

Based on the literature reviewed, it appears that HCHO causes hyperemia or inflammation in liver and kidney in rats. Macroscopic changes in the liver have also been produced by HCHO. When exposure is repeated over a period of weeks, changes include a mottled appearance and a decrease in liver weight.

Following a single high exposure, liver size may increase. Effects on viscera could result from indirect mechanisms or be secondary to other effects near the site of first contact. Transient effects on the hematopoietic system occurred in rats and mice after 6 months of exposure to HCHO by inhalation.

These effects were reflected by statistically significant decreases in 1 reticulocytes in female mice exposed to 2. This could indicate myeloid hyperplasia or erythroid hypoplasia. Thus, it is possible effects on visceral organs could be partially caused through changes in the hentatopoietic system as well as through other mechanisms IRMC, Introduction The sources of HCHO can be grouped into two major categories: direct or commercial production and indirect production.

The chemical is not imported in any appreciable quantities. Commercially, HCHO is produced from the catalytic oxidation of Methancl, using either silver oxide or a mixed-metal oxide as the catalyst. Processes accounting for the indirect production of HCHO include the photochemical oxidation of airborne hydrocarbons released from incomplete combustion processes, the direct production of HCHO during incomplete combustion of hydrocarbons in fossil fuels and refuse, and certain natural processes.

The commercial production of HCHO amounted to about 6 billion pounds. Adhesives and plastics are the major end uses. The "consumption" of HCHO can be broken down into three najor categories: nonconsumptive uses, pseudo-consumptive uses, and consumptive uses. In pseudo-consumptive uses, the chemical identity of HCHO does change, but it is not irreversibly altered. Under appropriate conditions, some or all of the original HCHO nay be regenerated. The derivatives are irreversibly formed and usually contain only residual levels of unreacted HCHO.

The major pseudo-consumptive uses are 1 urea-HCHO resins which are used in fiberboard, particleboard, plywood, laminates, urea-HCHO foams, molding compounds, and paper, textiles, and protective coatings; 2 urea-HCHO concentrates which are used to produce time-release fertilizers, and 3 hexamethylenetetramine which is used as a special anhydrous form of HCHO to cure resins and to treat textiles and rubber. The major consumptive uses are 1 melamine-HCHO resins which are used for molding compounds, fiberboard, particleboard, plywood, laminates, paper and textiles, 2 phenol-HCHO resins which are used in fiberboard, particleboard, plywood molding compounds, and insulation; 3 pentaerythritol which is used to produce alkyd resins, 4 1,4-butanediol which is used to produce tetrahydrofuran, 5 acetal resins which are used in the aanufacture of engineering plastics, and 6 trimethylolpropane which is used in the production of urethanes.

This study integrated the existing monitoring data, engineering or modeling estimates, use data, population estimates, and assessment of the likelihood of exposure from HCHO-related activities into an exposure assessment detailing those activities having a high HCHO exposure potential. The combined data were used as the basis for this risk assessment. Since specific monitoring data for all types of potentially exposed worker classifications or operational settings within an industry were generally not available, all workers in a given industry were assumed to be exposed to the mean exposure levels reported for that industry; in this case garment workers.

All worker exposure, however, is not in fact identical; worker exposure can vary because of the physical characteristics of the work site and the employee's work station for example. General population exposures conventional home residents were assumed to be for 70 years. Manufactured home residents were assumed to be exposed hours per week for 10 years. This is especially true for those populations or subpopulations for which little or no monitoring data are available and also for those populations for which the monitoring data were collected as a result of complaint investigations.

Populations at Risk As discussed previously the two populations at risk are certain home residents and garment workers. Home Residents The current population of relatively new manufactured homes is approximately 4,, This figure includes those people living in homes manufactured since Versar, However, prospective population estimates are also important. Based on a projection of manufactured housing starts by Versar a , it is estimated that 6,, persons will occupy a new manufactured home during the next ten years.

Garment Workers The number of potentially exposed garment workers is estimated to be , Versar, out of 1,, workers employed in the U. Summary Table presents population estimates for the two housing segments and garment manufacture. Assuming that the number of potentially exposed garment workers remains steady at ,, then a total of 47,, persons over the next ten years may have the potential to be affected by HCHO's noncancer effects.

In homes, these resins are used to bond the wood plys used to make plywood and to bind the wood particle and fibers used to make particleboard and medium density fiberboard. For garments, HCHO-baeed resins are used to impart permanent press finishes to the garments. Pressed-wood products Pressed-wood products are used in flooring, interior walls and doors, cabinetry, and furniture. The three principal types of products containing UF-resin are particleboard, medium-density fiberboard MDF , and hardwood plywood.

Particleboard is composition board comprised of 6 to 10 percent resin by weight , and small wood particles. UF resin is used in the majority of particleboard about 90 percent. The production of particleboard was over 3 billion square feet, of which 70 percent was used in furniture, fixtures,, cabinets, and similar products.

The remaining 30 percent is used for construction, including manufactured home manufacture common uses are as decking or flooring underlayment. MDF is also a composition board. It is comprised of wood fibers and 7 to 9 percent UF-resin.

Approximately 95 percent of MDF production over million square feet in was used to manufacture doors, fixtures, and cabinetry. Unlike the two composition boards discussed above, hardwood plywood is a laminated product; the resin is used as a glue to hold thin layers of wood and veneers together. The textiles normally treated are blends of cotton, acetate, and rayon. These fabrics account for percent of the textile produced annually. HCHO is released from treated fabric in three phases.

Release of HCHO by this mechanism is usually complete by the time garment workers receive the fabric. Surface desorption occurs during Phase II. This represents the release of HCHO which is not covalently bound to the fabric, and can last up to hours.

Phase III, in which hemiacetal hydrolysis is the mechanism of release, is thought to be the phase of HCHO release which results in worker exposure at the manufacturing site. That set product emission standards for particleboard 0. HUD believes that if the product standards are met and no other major emitters of formaldehyde are present e. Another study has reported average levels of 0. The Exposure Panel of the Workshop reported studies that showed average ambient levels of 0.

Thus, an unrealistic worst case exposure estimate was not used to estimate human risk.

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