Chemicals chronic effects

In the Green Screen the hazards of a chemical are defined by its potential to cause acute or chronic adverse effects in humans or wildlife, its fate in the environment, and certain physi-cal/chemical properties of concern to human health. Acute mammalian toxicity (lethality) and irritation of the skin or eye are examples of acute adverse effects that can result from inhalation, ingestion, or dermal contact with a chemical. Chronic effects occur after repeated exposures and include cancer and adverse effects to the reproductive, neurological, endocrine, or immune systems. 

In additional EPA studies, subchronic inhalation was evaluated ia the rat for 4 and 13 weeks, respectively, and no adverse effects other than nasal irritation were noted. In the above-mentioned NTP chronic toxicity study ia mice, no chronic toxic effects other than those resulting from bronchial irritation were noted. There was no treatment-related increase ia tumors ia male mice, but female mice had a slight increase in bronchial tumors. Neither species had an increase in cancer. Naphthalene showed no biological activity in other chemical carcinogen tests, indicating Htde cancer risk (44). No incidents of chronic effects have been reported as a result of industrial exposure to naphthalene (28,41). 

An exposure to a specific chemical in relatively low concentrations over a period may result in chronic effects. At higher concentrations, the effects may be acute. Some chemicals produce local damage at their point of contact with, or entry into, the body others produce systemic effects, i.e. they are transported within the body to various organs before exerting an adverse effect. 

Creosote is a complex mixture of toxic chemicals, which can have both immediate and chronic effects on exposed organisms. PIC of creosote are of particular concern due to long half-lives of some chemicals, and because of multiple pathways to the environment from ash and soot. 

Chronic Health Effect A chronic health effect is an adverse health effect resulting from long-term exposure to a substance. The effects could be a skin rash, bronchitis, cancer, or any other medical condition. An example would be liver cancer from inhaling low levels of benzene at your workplace over several years. The term is also applied to a persistent (months, years, or permanent) adverse health effect resulting from a short-term (acute) exposure. Chronic effects from long-term exposure to chemicals are fairly common. Recognize the PEL (permissible exposure level) for each substance in your workplace and minimize your exposure whenever possible. 

Late Toxicity - Where there is evidence that a chemical can cause cancer, mutagenic effects, teratogenic effects, or delayed injury to vital organs such as the liver or kidney, a qualitative description of the chemical is given. The term implies long-term or chronic effects due to exposure to the chemical. 

MRLs are derived for hazardous substances using the no-observed-adverse-effect level/uncertainty factor approach. They are below levels that might cause adverse health effects in the people most sensitive to such chemical-induced effects. MRLs are derived for acute (1-14 days), intermediate (15-364 days), and chronic (365 days and longer) durations and for the oral and inhalation routes of exposure. Currently, MRLs for the dermal route of exposure are not derived because ATSDR has not yet identified a method suitable for this route of exposure. MRLs are generally based on the most sensitive chemical-induced end point considered to be of relevance to humans. Serious health effects (such as irreparable damage to the liver or kidneys, or birth defects) are not used as a basis for establishing MRLs. Exposure to a level above the MRL does not mean that adverse health effects will occur. 

MRLs are derived for hazardous substances using the no-observed-adverse-effect level/uncertainty factor approach. They are below levels that might cause adverse health effects in the people most sensitive to such chemical-induced effects. MRLs are derived for acute (1-14 days), intermediate (15-364 days), and chronic (365 days and longer) durations and for the oral and inhalation routes of exposure. 

Chronic effects, however, arise from repeated exposures to low concentrations, mostly by small leaks. Many toxic chemical vapors are colorless and odorless (or the toxic concentration might be below the odor threshold). Small leaks of these substances might not become obvious for months or even years. There may be permanent and serious impairments from such exposures. Special attention must be directed toward preventing and controlling low concentrations of toxic gases. In these circumstances some provision for continuous evaluation is necessary that is, continuous or frequent and periodic sampling and analysis is important. 

Episodic pollution events can adequately be addressed by acute toxicity bioassays, however these are not sufficient to investigate the water quality for delayed toxicity effects of chemicals present. Chronic effects of pesticides can include carcinogenicity, teratogenicity, mutagenicity, neurotoxicity, and reproductive effects (endocrine disruption). 

Because notices for many new substances do not contain sufficient information and data for evaluating their toxicities (especially re chronic effects) and probable exposure patterns, EPA s primary focus in reviewing PMN s has been to determine whether it will request further testing. In some cases, the exercise (or threat of exercise) of the Agency s authority has proven sufficient to persuade a company either to hold up production of the substance voluntarily (while further data are developed), or to cease altogether its plans for bringing the chemical to market. 

In this paper I have tried to show that measurement of health benefits attributable to TSCA is not feasible. I hope that in doing so I have not belabored the obvious. For new chemicals and for most existing chemicals, prospective evaluation of health benefits to be achieved by various exposure controls will have to be based on extrapolation from microbial and animal data. However, while such extrapolation may be useful in a qualitative sense, quantitative risk assessment techniques involve considerable uncertainty, and in any case have not been developed for chronic effects other than cancer. 

Measurement or estimation of health impacts under TSCA would be premature, since relatively little has been done to regulate new or existing chemicals that could result in health benefits. The principal exception to this generalization is the ban on aerosol uses of CFCs, whose chronic effects on human health derive from their environmental impact rather than direct biological toxicity. Compared with other environmental laws, such as the Clean Air Act, the regulatory accomplishments of TSCA are somewhat insubstantial. 

First, one could observe that in the 2-1/2 years that the PMN program has been in effect there have been no known cases of people dropping dead because of a new chemical. This is not a very informative observation, however, because it is more a comment on the long latency period of chronic effects and our inability to detect chemical problems than it is an observation about the lack of problems with new chemicals. This is not to say that chemicals with adverse effects have gone through the PMN process—only that we would not know it if they had. 

---