Formaldehyde toxic effects

Daylight fluorescent pigments (qv) are considered to be nontoxic. Since they are combinations of polymers and dyestuffs, the combined effect of the ingredients must be taken into account when considering the net toxic effect of these materials. Table 5 gives results of laboratory animal toxicity tests of standard modified melamine—formaldehyde-type pigments, the Day-Glo A Series, and the products recommended for plastic mol ding, Day-Glo Z-series. 

Methanol is a dangerous fire hazard when exposed to heat or flame, and a moderate expl hazard when exposed to flame. It is a dangerous disaster hazard upon exposure to heat or flame, and can react vigorously with oxidizing materials. Methanol possesses distinct narcotic props, and is also a slight irritant to the mucous membranes. Its main toxic effect is exerted upon the nervous system, particularly the optic nerves and possibly the retinae. In the body the products formed by its oxidn are formaldehyde and formic acid, both of which are toxic. Because of the slowness with which it is eliminated, methanol should be regarded as a cumulative poison (Ref 5)... 

Maintaining the stability of a biological treatment of wastewaters containing formaldehyde and urea is complicated because some compounds exert a toxic effect on the processes involved. Figure 19.5 shows the possible toxic interactions between the different compounds and processes. 

The other major toxic effect of methanol is the ocular toxicity. Although formaldehyde might be formed locally in the retina, this seems unlikely, whereas formate is known to cause experimental ocular toxicity. The mechanism suggested involves inhibition by formate of cytochrome oxidase in the optic nerve. As the optic nerve cells have few mitochondria, they are very susceptible to this "histotoxic hypoxia,"... 

Methyl alcohol possesses distinct natcotic properties. It is also a slight irritant to ihe mucous membranes. The principal toxic effect is exerted on the nervous system, particularly the optic nerves and possibly Ihe relinae. The eflect upon the eyes has been attributed to optic neuritis, which subsides, but is followed by atrophy uf the optic nerve. Once absorbed, methyl alcohol is only very slowly eliminated. Coma resulting from massive exposures may last as long as 2 to 4 days. In the body, the paiducis formed hy its oxidation arc formaldehyde and formic acid, both of which are toxic. 

Ingestion of methanol, particularly during the prohibition era, resulted in significant illness and mortality. Where epidemics of methanol poisoning have been reported, one-third of the exposed population recovered with no ill effects, one-third have severe visual loss or blindness, and one-third have died. Methanol itself is not responsible for the toxic effects but is rapidly metabolized in humans by alcohol dehydrogenase to formaldehyde, which is subsequently metabolized by aldehyde dehydrogenase to form... 

The fact that formaldehyde is produced by natural processes in the environment and in the body would suggest that it might not be very toxic. However, such is not the case in that formaldehyde exhibits a number of toxic effects. 

Children are especially vulnerable to the toxic effects of aspartame probably because formaldehyde is totally intolerable to biological systems. 

Formaldehyde is an important industrial chemical for the production of synthetic resins. These resins are applied primarily as adhesives in the production of a large number of consumer products and construction materials that end up in homes. Other sources of indoor formaldehyde include urea-formaldehyde foam insulation, textile additives, as well as combustion and tobacco smoke. Formaldehyde is one of the many VOCs present indoors and it is considered the most abundant among them. It has important toxic effects in the 0.1-5 ppm concentration range. 

Intoxication may present as inebriation and drowsiness similar to ethanol use. Other symptoms are vomiting, diarrhea, delirium and agitation, back and abdominal pain, and clammy skin. Toxic effects usually follow a latent period of several hours. Formate inhibits mitochondrial cytochromes resulting in neurotoxicity. Ocular signs include blurred vision, dilated pupils, and direct retinal toxicity with optic disc hyperemia and ultimately permanent blindness [91]. Cerebral hemorrhagic necrosis has been reported [92]. Severe poisoning may result in Kussmaul respiration, inspiratory apnea, coma, and death. Urine samples may have the characteristic smell of formaldehyde. An elevated serum osmolal gap from methanol will be evident early in presentation but may disappear after approximately 12 hours. At this time, an elevated anion gap metabolic acidosis from retained formate may be evident. 

Not only can the toxicity of active substances be reduced by povidone. The irritant or toxic effects of other substances such as cyanides, nicotine, formaldehyde, formamide, and other toxins, with which povidone forms complexes of adequate stability, can also be reduced [126]. 

Formaldehyde is a major contributor to many cases of sick building syndrome. It is a very toxic chemical that is corrosive to the skin, eyes, and the respiratory system. Acute or chronic exposure can result in difficulty breathing and even brief exposures can induce asthmatic reactions in sensitized individuals. 13 Exposures to mixtures of formaldehyde and lipophilic chemicals can result in unanticipated toxic effects. 14 Formaldehyde is an animal carcinogen, a suspected human nasal cancer carcinogen 29 and suspected human leukemogen. 3°1... 

ACD has been associated with ethoxylated alcohol surfactants. Though not by themselves known to cause ACD, ethoxylated surfactants are polyethers and are easily air oxidized to hydroperoxides, peroxides, and carbonyl compounds (including formaldehyde and acetaldehyde), substances that do cause ACDJ22 251 The irritant components of surfactants and other chemicals present in formulated products facilitate the absorption of the ACD causing decomposition products of ethoxylated alcohols and thus exacerbate their effects. F61 This is yet another example of lipophilic compounds enhancing the absorption of hydrophilic compounds (the decomposition products of ethoxylated alcohols) and hence increasing the toxic effect beyond that predicted. 

No evidence for formaldehyde-induced effects on the skin has been reported in intermediate-duration inhalation studies with rats, hamsters. Rhesus monkeys, or mice (Appelman et al. 1988 Maronpot et al. 1986 Monticello et al. 1989 Woutersen et al. 1987), or in chronic inhalation studies with rats or mice (Kamata et al. 1997 Kems et al. 1983b), except that the highest concentration used in these studies (40 ppm used in the 13-week mouse study by Maronpot et al. 1986) produced severe clinical signs of toxicity in mice including mouth breathing, ataxia, and loss of skin elasticity . 

The toxicity of formaldehyde is route-dependent. Irritation at the point of contact is seen by inhalation, oral, and dermal routes. High doses are cytotoxic and result in degeneration and necrosis of mucosal and epithelial cell layers. These observations are consistent with the hypothesis that toxic effects are mediated by formaldehyde itself and not by metabolites. No specific target molecule has been identified, although DNA-protein cross links have been identified (Casanova and Heck 1987). As discussed in... 

Section 2.2, oral and inhalation toxicity studies with animals generally have found that toxic effects from formaldehyde are restricted to portal-of-entry tissue, but there are scattered reports of toxic effects at sites distant from portals-of-entry. The mechanism whereby distant site toxicity may be expressed is unclear, but given the highly reactive nature of formaldehyde and the ubiquitous metabolic capability of cells to metabolize formaldehyde, it is plausible that distant site effects may occur only when the capacity for local disposition of formaldehyde is exceeded. 

Studies of animals exposed for life to formaldehyde in air or drinking water also show that formaldehyde primarily damages tissue at portals-of-entry (i.e., the upper respiratory tract and the gastrointestinal tract) evidence for toxic effects at distant sites is less consistent. Replicated inhalation studies have shown that formaldehyde induced malignant nasal tumors in rats at high exposure concentrations (10-15 ppm) that also induced nasal epithelial necrosis and cellular proliferation, but not at lower concentrations (0.3-2 ppm) that did not markedly damage nasal epithelial tissue (Albert et al. 1982 ... 

A few controlled exposure studies have found only subtle or infrequent effects of formaldehyde on lower respiratory tract function in this concentration range, supporting the hypotheses that the upper respiratory tract is a more likely target of formaldehyde toxicity than the lower respiratory tract and that pulmonary hypersensitivity to formaldehyde is rare (Green et al. 1987 Nordman et al. 1985 Sauder et al. 1986). 

In general, the information from reports of acute poisoning in humans ingesting formaldehyde and reports of studies of animals exposed to formaldehyde in air, in drinking water, or in the diet indicate that the liver is not a prime target of formaldehyde toxicity, and that hepatic effects from exposure to... 

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