Public health implications of 1990 air toxics concentrations across the United States.

Occupational and toxicological studies have demonstrated adverse health effects from exposure to toxic air contaminants. Data on outdoor levels of toxic air contaminants have not been available for most communities in the United States, making it difficult to assess the potential for adverse human health effects from general population exposures. Emissions data from stationary and mobile sources are used in an atmospheric dispersion model to estimate outdoor concentrations of 148 toxic air contaminants for each of the 60,803 census tracts in the contiguous United States for 1990. Outdoor concentrations of air toxics were compared to previously defined benchmark concentrations for cancer and noncancer health effects. Benchmark concentrations are based on standard toxicological references and represent air toxic levels above which health risks may occur. The number of benchmark concentrations exceeded by modeled concentrations ranged from 8 to 32 per census tract, with a mean of 14. Estimated concentrations of benzene, formaldehyde, and 1,3-butadiene were greater than cancer benchmark concentrations in over 90% of the census tracts. Approximately 10% of all census tracts had estimated concentrations of one or more carcinogenic HAPs greater than a 1-in-10,000 risk level. Twenty-two pollutants with chronic toxicity benchmark concentrations had modeled concentrations in excess of these benchmarks, and approximately 200 census tracts had a modeled concentration 100 times the benchmark for at least one of these pollutants. This comprehensive assessment of air toxics concentrations across the United States indicates hazardous air pollutants may pose a potential public health problem.

The effect of pindolol and salmon calcitonin on experimental gastric ulcers in rats.

Many different experimental models for the induction of gastric ulcers have been reported in rats. Most of these experimental designs are often not reproducible and the interpretation of the results obtained is sometimes difficult. In the present study, three different models were found to give reliable and reproducible results, which could be repeated at any time of the year with different experimenters performing the procedure. To date, these methods are in our opinion, the best in designing gastric ulcer experiments and assessing the effect of pharmacological active substances. Two pharmacological active substances were investigated in the present study, pindolol, a beta-blocking agent with intrinsic sympathomimetic activity and salmon calcitonin, a hormone influencing calcium homeostasis in blood. Using all three different models no effect was seen after pindolol administration, while a strong inhibitory effect on the formation of gastric ulcers was observed after salmon calcitonin. Following ligation of the pylorus, the ulcer formation rate was significantly decreased from 80 to 33% with a significant fall in ulcer index from 2 to 0.42 and reduction of the ulcer areas from 6.6 to 0.58 mm2 (p less than 0.05). In addition, following phenylbutazone administration the appearance of gastric ulcers was diminished after salmon calcitonin from 1.4 to 0.43 and in ulcer area from 4.5 to 0.95 mm2 (p less than 0.01). These three ulcer models used in the present study were found to be very reliable as compared with other models reported in the literature and tested in our laboratory.

The politics of reproductive hazards in the workplace: class, gender, and the history of occupational lead exposure.

Over the past two decades, several U.S. companies have sought to bar women from jobs that expose them to potential reproductive hazards, justifying these exclusionary policies by their professed concerns for the well-being of unborn children and potential liability. Although recent court cases have stimulated academic interest in this issue, a historical review of the public health and medical literature reveals that this debate is not new. To understand the logic behind the emergence of "fetal protection" policies, one must examine the scientific history of occupational teratogens and the socio-political and economic forces that have driven scientific research in this field. Using lead as an example, the author argues that research on the reproductive hazards of employment has historically emphasized the risks to women and downplayed the risks to men. This results in environmental health policies that do not uphold the ultimate goal of occupational safety for all workers, but rather reinforce the systemic segregation of men and women in the workplace. Although the political struggle over exclusionary policies has a feminist orientation, it also has important class dimensions and ultimately must be viewed within the broader context of American capitalist production.

Industrial ecology: a philosophical introduction.

By analogy with natural ecosystems, an industrial ecology system, in addition to minimizing waste production in processes, would maximize the economical use of waste materials and of products at the ends of their lives as inputs to other processes and industries. This possibility can be made real only if a number of potential problems can be solved. These include the design of wastes along with the design of products and processes, the economics of such a system, the internalizing of the costs of waste disposal to the design and choice of processes and products, the effects of regulations intended for other purposes, and problems of responsibility and liability. The various stakeholders in making the effects of industry on the environment more benign will need to adopt some new behaviors if the possibility is to become real.

Air toxics and health risks in California: the public health implications of outdoor concentrations.

Of the 188 hazardous air pollutants (HAPs) listed in the Clean Air Act, only a handful have information on human health effects, derived primarily from animal and occupational studies. Lack of consistent monitoring data on ambient air toxics makes it difficult to assess the extent of low-level, chronic, ambient exposures to HAPs that could affect human health, and limits attempts to prioritize and evaluate policy initiatives for emissions reduction. Modeled outdoor HAP concentration estimates from the U.S. Environmental Protection Agency's Cumulative Exposure Project were used to characterize the extent of the air toxics problem in California for the base year of 1990. These air toxics concentration estimates were used with chronic toxicity data to estimate cancer and noncancer hazards for individual HAPs and the risks posed by multiple pollutants. Although hazardous air pollutants are ubiquitous in the environment, potential cancer and noncancer health hazards posed by ambient exposures are geographically concentrated in three urbanized areas and in a few rural counties. This analysis estimated a median excess individual cancer risk of 2.7E-4 for all air toxics concentrations and 8600 excess lifetime cancer cases, 70% of which were attributable to four pollutants: polycyclic organic matter, 1,3 butadiene, formaldehyde, and benzene. For noncancer effects, the analysis estimated a total hazard index representing the combined effect of all HAPs considered. Each pollutant contributes to the index a ratio of estimated concentration to reference concentration. The median value of the index across census tracts was 17, due primarily to acrolein and chromium concentration estimates. On average, HAP concentrations and cancer and noncancer health risks originate mostly from area and mobile source emissions, although there are several locations in the state where point sources account for a large portion of estimated concentrations and health risks. Risk estimates from this study can provide guidance for prioritizing research, monitoring, and regulatory intervention activities to reduce potential hazards to the general population. Improved ambient monitoring efforts can help clarify uncertainties inherent in this analysis.

Application of health information to hazardous air pollutants modeled in EPA's Cumulative Exposure Project.

Relatively little is known about the spectrum of health effects, and the scope and level of ambient air concentrations of those pollutants regulated under the Clean Air Act as "hazardous air pollutants". The U.S. Environmental Protection Agency's (USEPA) Cumulative Exposure Project uses currently available emissions inventories, from a variety of source types, and an atmospheric dispersion model to provide estimates of ambient concentrations for 148 hazardous air pollutants (HAPs) in over 60,000 census tracts for the year 1990. This paper uses currently available hazard information for those pollutants and provides a database of potential regulatory threshold concentrations of concern, or "benchmark concentrations," and a methodology for prioritizing and characterizing the quality of the data. In order to demonstrate application of the database and prioritization scheme to outputs from the Cumulative Exposure Project, comparisons were made with the maximum modeled concentration of each individual hazardous air pollutant across the census tracts. Of the 197 benchmark concentrations for cancer and non-cancer (long- and short-term exposures) effects compiled for the study, approximately one half were exceeded with a predominance of exceedance of cancer benchmarks. While the number of benchmark concentrations available to fully characterize potential health effects of these pollutants was limited (approximately 80 percent of HAPs identified as cancer concerns had benchmark concentrations for cancer and 50 percent of all HAPs had non-cancer benchmark concentrations) and there was greater uncertainty in derivation of maximum modeled air concentrations than other levels, the comparison between the two was a useful approach for providing an indication of public health concern from hazardous air pollutants.