Epidemiological Studies Of Workers Research Articles

The health risk of chrysotile asbestos.

The word asbestos is a poorly attributed term, as it refers to two very different minerals with very different characteristics. One is the serpentine mineral of which the white asbestos, chrysotile, is the most common. The other is the amphibole asbestos, which includes the blue asbestos crocidolite and the brown asbestos amosite. Although today chrysotile is the only type used commercially, the legacy of past use of amphibole asbestos remains. This review clarifies the differences between the two mineral families referred to as asbestos and summarizes the scientific basis for understanding the important differences in the toxicology and epidemiology of these two minerals. Biopersistence and sub-chronic inhalation toxicology studies have shown that exposure to chrysotile at up to 5000 times the current threshold limit value (0.1 fibers/cm) produces no pathological response. These studies demonstrate as well that following short-term exposure the longer chrysotile fibers rapidly clear from the lung and are not observed in the pleural cavity. In contrast, short-term exposure to amphibole asbestos results quickly in the initiation of a pathological response in the lung and the pleural cavity. Significant progress has been made in understanding the factors that influence inhalation toxicology studies of fibers and epidemiological studies of workers. Evaluation of the toxicology and epidemiology studies of chrysotile indicates that it can be used safely under controlled use. In contrast, even short-term exposure to amphibole asbestos can result in disease.

Reconstruction of historical exposures at a Welsh nickel refinery (1953-2000).

Past epidemiological studies of workers in a nickel refinery in Clydach, Wales, have shown evidence of large excess respiratory cancer mortality risks [lung cancer relative risk (RR) ≈ 3; nasal cancer RR ≈ 140] in those employed prior to 1930, with risks dropping dramatically in workers hired subsequently. The pre-1930 risks have generally been attributed to high exposures to mixtures of nickel compounds. More recent studies of this refinery's workers have focused on those first hired in 1953, when many of the operations that presumably gave rise to the high exposures were no longer in operation. While these studies have shown greatly decreased lung cancer risks overall (RR ≈ 1.4), and no substantive evidence of increased nasal cancer risk, the absence of reliable exposure estimates have made it difficult to ascertain whether the increased lung cancer risks are nickel related or due to other factors. This study uses nickel measurements from the 1970s to the present, documentation of process changes, and dust measurements taken around the 1950s to construct an exposure matrix for the recent cohort. It provides evidence of at least 30-fold decreases in levels of nickel exposure from the 1950s to the present, with estimated inhalable nickel concentrations in the 1950s in excess of 5mg Ni m(-3).

An updated inhalation unit risk factor for arsenic and inorganic arsenic compounds based on a combined analysis of epidemiology studies

The United States Environmental Protection Agency (USEPA) developed an inhalation unit risk factor (URF) of 4.3E-03 per μg/m3 for arsenic in 1984 for excess lung cancer mortality based on epidemiological studies of workers at two smelters: the Asarco smelter in Tacoma, Washington and the Anaconda smelter in Montana. Since the USEPA assessment, new studies have been published and exposure estimates were updated at the Asarco and Anaconda smelters and additional years of follow-up evaluated. The Texas Commission on Environmental Quality (TCEQ) has developed an inhalation URF for lung cancer mortality from exposures to arsenic and inorganic arsenic compounds based on a newer epidemiology study of Swedish workers and the updates of the Asarco and Anaconda epidemiology studies. Using a combined analysis approach, the TCEQ weighted the individual URFs from these three epidemiology cohort studies, to calculate a final inhalation URF of 1.5E-04 per μg/m3. In addition, the TCEQ also conducted a sensitivity analysis, in which they calculated a URF based on a type of meta-analysis, and these results compared well with the results of the combined analysis. The no significant concentration level (i.e., air concentration at 1 in 100,000 excess lung cancer mortality) is 0.067μg/m3. This value will be used to evaluate ambient air monitoring data so the general public in Texas is protected against adverse health effects from chronic exposure to arsenic.

Long-term Dietary Cadmium Intake and Cancer Incidence

Cadmium, a ubiquitous environmental pollutant, is classified as a carcinogenic substance. Several laboratory and epidemiologic studies of workers and subjects in polluted areas have suggested a positive association between cadmium exposure and risk of several cancers. However, data from general populations are sparse. We prospectively examined the association between cadmium exposure and incidence of cancer in a Japanese population with a relatively high dietary intake of cadmium. We conducted a population-based prospective study in 90,383 Japanese men and women 45-74 years of age. Participants responded to a validated questionnaire that included 138 food items. We estimated dietary cadmium intake from 6 food groups, based on the questionnaire data. During 9 years of follow-up, 5849 cancer cases were identified. Hazard ratios (HRs) and 95% confidence intervals (CIs) for cancer were calculated by Cox proportional hazards modeling. There was no evidence of an association of cadmium consumption and total cancer, with HRs in the highest versus lowest cadmium intake group of 0.94 (95% CI = 0.82 to 1.08; test for trend, P = 0.46) for men and 0.96 (0.81 to 1.15; 0.60) for women. No site-specific cancers were associated with cadmium intake in men or women. We found no associations of cancer with cadmium, at least at the exposure levels observed in a general population in Japan.

Comparing single and repeated dosimetry data for perfluorooctane sulfonate in rats

Perfluorooctane sulfonate (PFOS) is a member of a class of perfluorinated chemicals used in a variety of consumer and industrial applications because of their oleophobic and hydrophobic properties. It has been shown to cause toxicity in adult and developing laboratory animals. Because PFOS has also been shown to be widely distributed throughout the environment, there have been concerns about its potential health risk to humans. Limited pharmacokinetic data for PFOS are available in rodents and humans, while epidemiological studies of workers and extensive toxicity studies in rodents have been performed. The existing pharmacokinetic and toxicity database in rodents can be useful in the cross-species extrapolations needed to evaluate and interpret internal dosimetry in humans. A mathematical model that describes the disposition of PFOS in adult rats following intravenous, oral, and chronic dietary exposures was developed to gain a better understanding of the pharmacokinetics of PFOS and to determine whether single-dose kinetics are predictive of repeated-dose kinetics. In order to characterize existing time-course data, time-dependent and concentration-dependent changes in the pharmacokinetic parameters for urinary and biliary clearance and liver distribution were needed. Whether these time-dependent changes represent inconsistencies across experiments, effects of aging in the rats, or chemically induced changes in pharmacokinetics remains to be determined.

Quantitative assessment of neuromotor function in workers with current low exposure to mercury vapor

Evaluation of neuromotor function has been used in several epidemiological studies of workers with long-term exposure to mercury vapor (Hg 0). Some recent studies indicate adverse effects at relatively low exposure levels. In the present study, we used sensitive quantitative methods, developed specifically to detect subtle effects of exposure to toxins on motor function. After exclusion of individuals with neurological diseases or other conditions that may affect performance, 43 chloralkali workers with current low exposure to Hg 0, and 22 age-matched referents remained for further analysis. The median urinary mercury concentration in exposed workers was 5.9 μg/g (range 1.3–25) creatinine (μg/gC), while that in referents was 0.7 μg/gC (range 0.2–4.1). The mean exposure time was 15 years, and the median cumulative mercury index was 161 years × μg/gC in exposed workers. A eurythmokinesimeter (EKM) was used to quantify eye–hand coordination, and a diadochokinesimeter, to measure rapid alternating rotation of the forearms. In general, the differences in performance between the exposed workers and the referents were small. Age was associated with a decrease in speed, more tremor, and longer contact duration between the stylus and the metal targets in performance of rapid pointing movements. Smokers had significantly more tremor, and more contacts per event in the EKM test, than nonsmokers. Taking age, shift work, and smoking habits into account, no significant associations with current or cumulative mercury exposure were found for the majority of the outcome variables from the quantitative tests. In general, this study indicates no significant adverse effects of Hg 0 on neuromotor function at the exposure levels studied.

Quantitative Assessment of Neuromotor Function in Workers With Current Low Exposure to Mercury Vapor

Evaluation of neuromotor function has been used in several epidemiological studies of workers with long-term exposure to mercury vapor (Hg 0). Some recent studies indicate adverse effects at relatively low exposure levels. In the present study, we used sensitive quantitative methods, developed specifically to detect subtle effects of exposure to toxins on motor function. After exclusion of individuals with neurological diseases or other conditions that may affect performance, 43 chloralkali workers with current low exposure to Hg 0, and 22 age-matched referents remained for further analysis. The median urinary mercury concentration in exposed workers was 5.9 microg/g (range 1.3-25) creatinine (microg/gC), while that in referents was 0.7 microg/gC (range 0.2-4.1). The mean exposure time was 15 years, and the median cumulative mercury index was 161 years x microg/gC in exposed workers. A eurythmokinesimeter (EKM) was used to quantify eye-hand coordination, and a diadochokinesimeter, to measure rapid alternating rotation of the forearms. In general, the differences in performance between the exposed workers and the referents were small. Age was associated with a decrease in speed, more tremor, and longer contact duration between the stylus and the metal targets in performance of rapid pointing movements. Smokers had significantly more tremor, and more contacts per event in the EKM test, than nonsmokers. Taking age, shift work, and smoking habits into account, no significant associations with current or cumulative mercury exposure were found for the majority of the outcome variables from the quantitative tests. In general, this study indicates no significant adverse effects of Hg 0 on neuromotor function at the exposure levels studied.

Isocyanate Exposures in Autobody Shop Work: The SPRAY Study

Isocyanates, known to cause respiratory sensitization and asthma, are widely used in automotive refinishing where exposures to aliphatic polyisocyanates occur by both inhalation and skin contact. The work reported here, the characterization of isocyanate exposure in the autobody industry, was part of an epidemiologic study of workers in 37 autobody shops in Connecticut. This article describes workplaces, tasks, and controls, and outlines the frequency, duration, and intensity of isocyanate exposures. Personal air samples taken outside of respirators had median concentrations of 66.5 μg NCO/m3 for primer, 134.4 μg (NCO)/m3 for sealer, and 358.5 μg NCO/m3 for clearcoat. Forty-eight percent of primer, 66% of sealer, and 92% of clearcoat samples exceeded the United Kingdom Health and Safety Executive guideline for isocyanate, though none exceeded the National Institute for Occupational Safety and Health (NIOSH) recommended exposure limit for monomer. Nonisocyanate-containing primers and sealers are used in more than half the shops, but nonisocyanate clearcoats are rare. Eighty-two percent of personal samples taken within a spray booth exceeded the U.K. guideline: 81% of those in downdraft spray booths, 74% in semidowndraft booths, and 92% in crossdraft booths. Only 8% of shops reported that spraying is done exclusively in spray booths. All painters wore some type of respirator. In 30% of shops, painters used supplied air respirators; the rest relied on half face organic vapor cartridge respirators with N95 overspray pads. All shops provided some type of gloves, usually latex, not recommended for isocyanate protection. Despite improvements in autobody shop materials, practices, and controls, there are still opportunities for substantial exposures to isocyanates.

Nickel Carcinogenicity in Relation to the Health Risks from Residual Oil Fly Ash

ABSTRACT Epidemiological studies of workers in the nickel industry, animal exposure studies, and reports on the potential mechanisms of nickel-induced toxicity and carcinogenicity indicate that only crystalline sulfidic nickel compounds have been clearly established as carcinogenic or potentially carcinogenic in humans. This observation indicates the need to modify and update regulatory approaches for nickel to reflect noncancer toxicity values for some individual nickel species. Analysis of nickel compounds in residual oil fly ash (ROFA) indicates that sulfidic nickel compounds (e.g., nickel subsulfide, nickel sulfide) are not present. Thus, the potential for emission of carcinogenic nickel compounds from residual oil fly ash appears to be low. Preliminary reference concentrations (RfCs) for a number of nickel compounds, based on non-carcinogenic endpoints, are proposed on the basis of the benchmark dose approach in conjunction with NTP data for nickel species.

Alteration in Cellular and Biochemical Markers of Pulmonary Toxicity in Rat Lung Exposed to Carpet Dusts

Epidemiological studies of workers in weaving units in carpet industries have shown relationships between the airborne dust concentrations and pulmonary ill health. Therefore, to predict the health risk of carpet weavers, this preliminary experiment was conducted to evaluate the effect of carpet dust (knotted, tufted) on cellular and biochemical mediators considered as potential biological markers of lung injury. Lung cytoplasmic (lactate dehydrogenase, LDH), lysosomal (acid phosphatase, ACP), type II (alkaline phoshatase, ALP) and Clara-cell marker enzymes (gamma-glutamyl transferase, GGT) were monitored in rat cell-free lung lavage (BAL) during postexposure days 1, 4, 8, and 16. Furthermore, lung microsomal cytochrome P-450 (CYP450) and Clara-cell secretory protein (CC16) content in BAL was also evaluated. These pulmonary marker enzymes were significantly elevated during the postexposure period over the respective untreated control; however, tufted carpet dust shows more responses than knotted carpet dust. Lung CYP450 content was reduced significantly at early days; the pattern shows the reoccurrence of CYP450 content in the later stage of postexposure to carpet dust. Clara-cell secretory protein in BAL shows decline in the carpet-treated group; however, tufted carpet shows more decline than knotted carpet. Thus, reduction in CC16 level may have important implication in the development of chronic lung inflammation and diseases. Present investigation found that modulation of these cellular marker enzymes is clear evidence of pulmonary damage caused by exposure to carpet dust.

Differential responses of rat alveolar macrophages to carpet dust in vitro.

Epidemiological studies of workers in carpet weaving units in carpet industries have shown a direct relation between the concentration of carpet dust in the air and respiratory symptoms. To predict the health risk of carpet weavers, this preliminary study was conducted to evaluate the toxic potential of different types of workplace dust by using alveolar macrophages (AMs). Several parameters were observed for cytotoxicity such as cell viability, the release of lactate dehydrogenase (LDH) in rat AMs treated with different concentration of carpet dust and haemolytic potential of erythrocytes. In addition, reactive oxygen/nitrogen species-inducing effects of carpet dust were assessed by nitric oxide (NO), reduced glutathione (GSH) release and hydrogen peroxide (H2O2) generation in AMs. Results of cell viability and hemolytic assay showed a direct correlation between increasing the dust concentration with enhancing the toxic effect. Knotted and tufted carpet dust increases the release of LDH, NO, GSH and H2O2 production with increasing dust concentration. Present observations have revealed that dusts collected from tufted carpet weaving units exhibited more toxicity to AMs than knotted carpet dust. These data further suggest that injurious effects of carpet dust to AMs could pave a way to evaluate the toxic potential of the different types of workplace dusts and component(s) involved in it.

Alteration in Cellular and Biochemical Markers of Pulmonary Toxicity in Rat Lung Exposed to Carpet Dusts

Epidemiological studies of workers in weaving units in carpet industries have shown relationships between the airborne dust concentrations and pulmonary ill health. Therefore, to predict the health risk of carpet weavers, this preliminary experiment was conducted to evaluate the effect of carpet dust (knotted, tufted) on cellular and biochemical mediators considered as potential biological markers of lung injury. Lung cytoplasmic (lactate dehydrogenase, LDH), lysosomal (acid phosphatase, ACP), type II (alkaline phoshatase, ALP) and Clara-cell marker enzymes (gamma-glutamyl transferase, GGT) were monitored in rat cell-free lung lavage (BAL) during postexposure days 1, 4, 8, and 16. Furthermore, lung microsomal cytochrome P-450 (CYP450) and Clara-cell secretory protein (CC16) content in BAL was also evaluated. These pulmonary marker enzymes were significantly elevated during the postexposure period over the respective untreated control; however, tufted carpet dust shows more responses than knotted carpet dust. Lung CYP450 content was reduced significantly at early days; the pattern shows the reoccurrence of CYP450 content in the later stage of postexposure to carpet dust. Clara-cell secretory protein in BAL shows decline in the carpet-treated group; however, tufted carpet shows more decline than knotted carpet. Thus, reduction in CC16 level may have important implication in the development of chronic lung inflammation and diseases. Present investigation found that modulation of these cellular marker enzymes is clear evidence of pulmonary damage caused by exposure to carpet dust.

CARBON DISULFIDE: HAZARD CHARACTERIZATION AND EXPOSURE-RESPONSE ANALYSIS

Carbon disulfide has been assessed as a Priority Substance under the Canadian Environmental Protection Act. Based on the results of epidemiological studies of workers exposed to carbon disulfide and supporting data from experiments conducted on animals, the nervous system appears to be the critical target for carbon disulfide-induced toxicity, manifested most often as reduced conduction velocity in the peripheral nerves and impaired performance in psychomotor testing. Other effects for which there is considerable weight of evidence in humans exposed to carbon disulfide include alterations in serum lipids and blood pressure that are associated with increased risk of heart disease, damage to the blood vessels of the retina and (with higher exposures) increased mortality from heart disease. A tolerable concentration of 100 μg/m3 has been derived, based upon the benchmark concentration associated with a 5% adverse response for the most sensitive response variable (i.e., peroneal motor nerve conduction velocity at 20 mg/m3) in an epidemiological study of an occupationally exposed population.

Risks of fatal cancer from inhalation of 239,240plutonium by humans: a combined four-method approach with uncertainty evaluation.

The risk per unit dose to the four primary cancer sites for plutonium inhalation exposure (lung, liver, bone, bone marrow) is estimated by combining the risk estimates that are derived from four independent approaches. Each approach represents a fundamentally different source of data from which plutonium risk estimates can be derived. These are: (1) epidemiologic studies of workers exposed to plutonium; (2) epidemiologic studies of persons exposed to low-LET radiation combined with a factor for the relative biological effectiveness (RBE) of plutonium alpha particles appropriate for each cancer site of concern; (3) epidemiologic studies of persons exposed to alpha-emitting radionuclides other than plutonium; and (4) controlled studies of animals exposed to plutonium and other alpha-emitting radionuclides extrapolated to humans. This procedure yielded the following organ-specific estimates of the distribution of mortality risk per unit dose from exposure to plutonium expressed as the median estimate with the 5th to 95th percentiles of the distribution in parentheses: lung 0.13 Gy(-1) (0.022-0.53 Gy(-1)); liver 0.057 Gy(-1) (0.011-0.47 Gy(-1)); bone 0.0013 Gy(-1) (0.000060-0.025 Gy(-1)); bone marrow (leukemia), 0.013 Gy(-1) (0.00061-0.05 Gy(-1)). Because the different tissues do not receive the same dose following an inhalation exposure, the mortality risk per unit intake of activity via inhalation of a 1-microm AMAD plutonium aerosol also was determined. To do this, inhalation dose coefficients based on the most recent ICRP models and accounting for input parameter uncertainties were combined with the risk coefficients described above. The following estimates of the distribution of mortality risk per unit intake were determined for a 1-microm AMAD plutonium aerosol with a geometric standard deviation of 2.5: lung 5.3 x 10(-7) Bq(-1) (0.65-35 x 10(-7) Bq(-1)), liver 1.2 x 10(-7) Bq(-1) (0.091-20 x 10(-7) Bq(-1)), bone 0.11 x 10(-7) Bq(-1) (0.0030-4.3 x 10(-7) Bq(-1)), bone marrow (leukemia) 0.049 x 10(-7) Bq(-1) (0.0017-0.59 x 10(-7) Bq(-1)). The cancer mortality risk for all sites was estimated to be 10 x 10(-7) Bq(-1) (2.1-55 x 10(-7) Bq(-1))--a result that agrees very well with other recent estimates. The large uncertainties in the risks per unit intake of activity reflect the combined uncertainty in the dose and risk coefficients.

Cancer dose-response modeling of epidemiological data on worker exposures to aldrin and dieldrin.

The paper applies classical statistical principles to yield new tools for risk assessment and makes new use of epidemiological data for human risk assessment. An extensive clinical and epidemiological study of workers engaged in the manufacturing and formulation of aldrin and dieldrin provides occupational hygiene and biological monitoring data on individual exposures over the years of employment and provides unusually accurate measures of individual lifetime average daily doses. In the cancer dose-response modeling, each worker is treated as a separate experimental unit with his own unique dose. Maximum likelihood estimates of added cancer risk are calculated for multistage, multistage-Weibull, and proportional hazards models. Distributional characterizations of added cancer risk are based on bootstrap and relative likelihood techniques. The cancer mortality data on these male workers suggest that low-dose exposures to aldrin and dieldrin do not significantly increase human cancer risk and may even decrease the human hazard rate for all types of cancer combined at low doses (e.g., 1 microgram/kg/day). The apparent hormetic effect in the best fitting dose-response models for this data set is statistically significant. The decrease in cancer risk at low doses of aldrin and dieldrin is in sharp contrast to the U.S. Environmental Protection Agency's upper bound on cancer potency based on mouse liver tumors. The EPA's upper bound implies that lifetime average daily doses of 0.0000625 and 0.00625 microgram/kg body weight/day would correspond to increased cancer risks of 0.000001 and 0.0001, respectively. However, the best estimate from the Pernis epidemiological data is that there is no increase in cancer risk in these workers at these doses or even at doses as large as 2 micrograms/kg/day.

Updated Mortality Analyses of Pernis Epidemiological Data on Human Exposures to Aldrin and Dieldrin

An extensive clinical and epidemiological study of workers engaged in the manufacturing and formulation of aldrin and dieldrin, the Pernis study, provides occupational hygiene and biological monitoring data on individual exposures over the years of employment and provides the opportunity to investigate dose response relationships for these chemicals. The human epide miological mortality data on these workers, who were exposed to fairly substan tial lifetime average daily doses of aldrin and dieldrin, suggest that low dose exposures do not significantly increase human mortality and may even de crease the human mortality hazard rate. While hormesis from low dose expo sure to aldrin and dieldrin is not statistically significant, it is observed in the raw data and in the best fitting dose response models. The decrease in risk suggests increased survival time at low doses of aldrin and dieldrin. Using an upper bound on cancer potency based on mouse liver tumors, the U.S. Environmental Protection Agency (EPA) estimated that lifetime average daily doses (LADDs) of 0.0000625 and 0.00625 µg/kg body weight/day would correspond to increased cancer risks of 0.000001 and 0.0001, respectively. However, the best estimate from the Pernis epidemiological data is that LADDs of 0.0000625 and 0.00625 µg/kg body weight/day correspond to no increase in cancer risk and a decrease in the probability of mortality from all causes by the age of 70 years. At low doses of aldrin and dieldrin, the estimated decrease in mortality in a reference period of 70 years is more than 1000 times larger than the U.S. EPA's upper bound on the increase in the lifetime probability of cancer.

Validity of subjective assessment of changes in respiratory health status: a 30 year epidemiological study of workers in Paris.

The validity of scales used for subjective assessment of health, particularly transitional indices, is under discussion. The aim of the present study was to assess the concurrent and predictive validity of a simple estimate of long-term subjective assessment of respiratory health changes. A longitudinal study of 915 workers was conducted over 30 yrs, with both retrospective self-assessment of respiratory health changes and objective measurements of spirometric values 12 yrs apart. An assessment of the reason for death during the subsequent 20 yrs was performed. Subjective assessment of respiratory deterioration over 12 yrs was significantly related to both cross-sectional lung function values and longitudinal lung function changes (forced expiratory volume in one second (FEV1) decline), an association which remained after adjustment for FEV1 level. It was also related to the same risk factors as decline in FEV1 (smoking, occupational exposure). Self-evaluation of respiratory deterioration was significantly predictive of death from all causes, with the highest (but nonsignificant) rate ratio for respiratory causes. Asthmatics exhibited greater long-term variability (objective and subjective) than nonasthmatics. Independent of dyspnoea, self-assessment of respiratory health deterioration was significantly related to FEV1. Subjective assessment of long-term changes in respiratory health provides valid information.

The carcinogenicity of metals in humans.

Epidemiologic evidence on the relation between exposure to metals and cancer is reviewed. Human exposure to metals is common, with wide use in industry and long-term environmental persistence. Historically, the heaviest metal exposures occurred in the workplace or in environmental settings in close proximity to industrial sources. Among the general population, exposure to a number of metals is widespread but generally at substantially lower levels than have been found in industry. The carcinogenicity of arsenic, chromium, and nickel has been established. Occupational and environmental arsenic exposure is linked to increased lung cancer risk in humans, although experimental studies remain inconclusive. Experimental studies clearly demonstrate the malignant potential of hexavalent(VI) chromium compounds, with solubility being an important determining factor. Epidemiologic studies of workers in chromium chemical production and use link exposure to lung and nasal cancer. Experimental and epidemiologic data show that sparingly-soluble nickel compounds and possibly also the soluble compounds are carcinogens linked to lung and nasal cancer in humans. Some experimental and epidemiologic studies suggest that lead may be a human carcinogen, but the evidence is inconclusive. Although epidemiologic data are less extensive for beryllium and cadmium, the findings in humans of excess cancer risk are supported by the clear demonstration of carcinogenicity in experimental studies. Other metals, including antimony and cobalt, may be human carcinogens, but the experimental and epidemiologic data are limited.

Epidemiology of Work-Related Musculoskeletal Disorders

Musculoskeletal disorders are common in the United States. Although precise estimates are not available, most researchers agree that exposure to a combination of work place risk factors is a major contributor to these disorders. Along with personal factors (age, gender, etc.). Epidemiologic studies of workers have associated these disorders with many work-place physical and psychosocial factors. Specific physical factors associated with these disorders include intense, repeated, or sustained exertions, awkward, sustained, or extreme postures of the body, insufficient recovery time, vibration, and cold temperatures. Specific examples of work-place psychosocial factors include monotonous work, time pressure, high work load, lack of peer support, and a poor supervisor-employee relationship.

The toxicity of silicon carbide whiskers, a review

Abstract Epidemiological studies of workers occupationally exposed to man‐made mineral fibers have revealed a significant connection between exposure and the incidence of pulmonary pathologies including cancer. Although surface chemistry and related characteristics are factors in particle toxicity, most workers agree that the strongest correlate with toxicity is particle size and geometry. From the perspective of data available from exposure in animal models and in vitro experiments, one might expect silicon carbide whiskers to be at least as toxic as crocidolite asbestos. In several studies of workers involved in the production of SiC, fibers of silicon carbide were found associated with permanent respiratory dysfunction and lung cancer. Until competent studies of adequate duration in animal models are performed or epidemiological evidence is collected, a “no effect”; level can not be established. Measures should be taken in the work place to prevent pulmonary exposure to silicon carbide in fiber or whis...