[Combined effect of atmospheric pollution, occupational exposure, and tobacco habits in obstructive lung diseases. 3. Effects of occupational exposure].
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Occupational exposure limits (OELs) are tools to help employers protect the health of those who may be exposed to chemicals in their workplace. Under the United Kingdom Control of Substances Hazardous to Health (COSHH) Regulations they define adequate control by inhalation. OELs are set by the Health and Safety Commission (HSC) on advice from its Advisory Committee on Toxic Substances (ACTS) and after public consultation. Thus they are consensus limits which have the support of both sides of industry. COSHH uses two types of occupational exposure limit-the occupational exposure standard (OES) and the maximum exposure limit (MEL). OESs are set for substances for which it is possible to identify a concentration at which there is no significant risk to health. Employers are required to meet the limit, there is no requirement to go below it, and it can be exceeded provided steps are taken to meet it as soon as reasonably practicable. MELs are set for substances which have serious health implications and for which an OES cannot be set. Most of the substances with MELs are either carcinogens or causes of occupational asthma. Employers must not exceed an MEL and must reduce exposure as far below it as is reasonably practicable. MELs are set at concentrations achievable by good occupational hygiene practice such that risks to workers are judged to be reduced to a tolerable level. The HSC consider that this approach is preferable to the use of mathematical models to generate risk estimates, which inevitably gives a spurious appearance of accuracy. The MEL/OES system is poorly understand by many employers who use chemicals, is not comprehensive as some substances meet neither the OES nor MEL criteria, and does not mesh well with indicative occupational exposure limit values which will increasingly be set under the European Union Chemical Agents Directive. COSHH essentials: easy steps to control chemicals provides the practical help that firms need to control chemicals. It takes users straight from hazard and exposure considerations to benchmark standards of good practice. The problems with the current system have prompted ACTS to set up a subgroup to review the OEL framework.
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Occupational exposure to lead is widespread in the United States. Clinically evident lead poisoning as well as subclinical toxicity occur in populations with occupational lead exposure. The focus of current research on lead toxicity in industrial populations is in the definition of dose-response relationships, particularly at low levels of exposure. Major interest surrounds the development of biochemical and physiologic markers of subclinical toxicity. Need exists to better delineate the toxicity of lead on the peripheral and central nervous system, the kidneys, the cardiovascular system, and the reproductive organs using newly developed markers. To obtain more accurate information on cumulative individual exposure to lead, future research on lead toxicity will increasingly use X-ray fluorescence analysis for determination of the lead content in home.
Accurate exposure assessment remains a challenge in occupational epidemiology. We evaluated one approach, use of a job-exposure matrix (JEM), by applying the National Institute for Occupational Safety and Health (NIOSH) JEM to a large case-control birth defects study that included parental occupation information. We investigated the JEM exposure predictions in several ways and found that for a substantial proportion of the parents in the birth defects study, the JEM yielded either no exposure data or nonsense predictions. Among exposure predictions that were plausible, most were of low probability. The high probability exposure predictions were statistically unstable, and neither low nor high probability exposure predictions were reliable. There was considerable discrepancy between the JEM predictions and expert assessments for five exposures of interest. Application of the NIOSH JEM to the birth defects study database (and probably other databases as well) does not provide a useful means of assessing occupational exposures.
The risk of lung cancer in smokers was examined based on the debrisoquine metabolic phenotype and on exposure to occupational lung carcinogens, specifically asbestos and polycyclic aromatic hydrocarbons. Extensive metabolizers of debrisoquine are at a 4-fold increased risk for lung cancer compared to poor metabolizers, after adjustment for age, sex, and smoking (pack-years), when only occupationally unexposed subjects are considered. Increased risk related to the debrisoquine metabolic phenotype was greatest for squamous and small cell histologies, and least for the adenocarcinoma subtype. Men with a history of exposure to occupational carcinogens had significantly increased risk of lung cancer (relative risk = 2.8), after adjustment for age and smoking. Considering the combined effect of the high risk extensive metabolizers debrisoquine metabolic phenotype and likely occupational exposure to asbestos, the relative excess risk for lung cancer was 18-fold. This finding is consistent with a synergism in risk between the ability to extensively metabolize debrisoquine and occupational exposure to lung carcinogens in male smokers. Debrisoquine phenotyping has potential for identifying carcinogen-exposed workers at high risk of lung cancer.
Occupational asthma may account for a significant proportion of adult-onset asthma, but incidence estimates from surveillance of physician reports and workers' compensation data (0.9 to 15/100,000) are lower than expected from community-based cross-sectional studies of asthma patients. We conducted a prospective cohort study of 79,204 health maintenance organization members between the ages of 15 and 55 at risk for asthma. Computerized files, medical records, and telephone interviews were used to identify and characterize asthma cases. Evidence for asthma attributable to occupational exposure was determined from work-related symptoms and workplace exposure. The annual incidence of clinically significant, new-onset asthma was 1.3/1,000, and increased to 3.7/1,000 when cases with reactivation of previously quiescent asthma were included. Criteria for onset of clinically significant asthma attributable to occupational exposure were met by 21% (95% CI 12-32%) of cases giving an incidence of 71/100,000 (95% CI 43-111). Physicians documented asking about work-related symptoms in 15% of charts, and recorded suggestive symptoms in three cases, but did not obtain occupational medicine consultation, diagnose occupational asthma, report to the state surveillance program, or bill workers' compensation for any of them. These data suggest that the incidence of asthma attributable to occupational exposures is significantly higher than previously reported, and accounts for a sizable proportion of adult-onset asthma.
Occupational exposure information obtained via a questionnaire to close relatives of 160 deceased smelter workers was compared with data from employee registers. The data from the questionnaire regarding employment at the smelter had a very high validity, ie, a sensitivity of 98% and a specificity of 99%. When an assessment of arsenic exposure was made from information in the questionnaire, the sensitivity was only 40%, but the specificity was over 90%. Data on smoking habits were available from medical files for only 14 of the subjects. For all 14, the information was identical to the data in the questionnaires. It appears that questionnaires may sometimes be of use for exposure assessments in occupational health epidemiology.
1,3-Butadiene (BD) is an important industrial chemical and environmental contaminant, e.g. in urban air, traffic exhausts and tobacco smoke. It has been shown to be genotoxic in vitro and in vivo and carcinogenic in rodents, mice being more sensitive than rats. The present study confirmed this species difference. Using micronuclei in erythrocytes or bone marrow as a marker, mice responded at an effective level of 50 p.p.m., while the highest ineffective level in rats was 500 p.p.m. (inhalation of BD for 5 days). A dose-dependent increase in N-terminal valine haemoglobin adducts was seen in both rats and mice, but the adduct levels in the latter species were on average five times higher. For the first time, specific N6-alkyldeoxyadenosine adducts were identified in lung and liver DNA of rats exposed to BD by inhalation. No significant difference in DNA adduct level was seen in lung tissue of rats and mice at similar exposure levels. Occupational exposure levels to BD in the European Process industry are variable, but generally < 1 p.p.m. Haemoglobin adduct levels were seen to be increased among the worker groups with higher potential exposure to BD (process work, bomb voiding and repair duties) as compared with adduct levels in less exposed workers in maintenance and the laboratory or control personnel. However, the N-terminal valine haemoglobin adducts measured in the workers were one to two orders of magnitude lower than extrapolated for the same exposure dose in mice. In the same workers no exposure-related effects were seen in the cytogenetic parametres studied, i.e. chromosomal aberrations, sister chromatid exchanges or micronuclei in peripheral blood lymphocytes, or in the Ras oncoprotein levels of plasma samples. The studies so far conducted suggest that human exposure at the levels seen in the present day process industry can be documented at the biological dose level using haemoglobin adduct measurement, but not at the biological effect level using cytogenetic biomarkers. In order to quantitate the human genotoxic risk of BD exposure more work needs to be done on the role of other active BD metabolites than 1,2-epoxy-3-butene and on the genetic polymorphisms controlling the variability of individual responses.
Occupational exposure to blood borne pathogens has led to HBV, HCV and HIV infections among surgeons, nurses and other operating room (OR) personnel and, to a lesser degree, patients (Ross et al 2000, The incident investigation teams and others 1997). Of seven OR studies in which an observer or circulating nurse recorded exposures, there was a percuataneous injury in 1.7-15% of all surgeries, and a mucocutaneous contamination in 6.2-50% of all surgeries. (Gerberding et al 1990, Panlilio et al 1991, Popejoy & Fry 1991, Quebbeman et al 1991, Tokars et al 1992, Lynch & White 1993, Stringer, Infante-Rivard & Hanley 2002). Surgeons and residents usually sustained the greatest number of percutaneous and other exposures during surgery.
RATIONALE: Occupational exposures to vapors, gas, dust, or fumes have been shown to be a risk factor of airway obstruction in cross-sectional studies in the general population. OBJECTIVES: Our aim was to study the relationships between specific occupations and occupational exposures during a 9-yr follow-up period and changes in lung function and symptoms of chronic bronchitis. METHODS: Subjects from the general population aged 20 to 45 yr were randomly selected in 1991-1993 within the European Community Respiratory Health Survey. Follow-up took place from 1998 to 2002 among 4,079 males and 4,461 females in 27 study centers. A total of 3,202 men and 3,279 women twice completed lung function measurements. Job history during follow-up was linked to a job exposure matrix and consequently translated into cumulative exposure estimates. MAIN RESULTS: Individuals exposed to dusts, gases, and fumes during the period of follow-up did not have a steeper decline of FEV1 than did individuals with consistently white-collar occupations without occupational exposures (relative change among men and women, + 1.4 and -3.1 ml/yr, respectively; p > 0.2), nor an increase of prevalence or incidence of airway obstruction defined as an FEV1/FVC ratio of less than 0.7. The incidence of chronic phlegm increased in men exposed to mineral dust (relative risk, 1.94 [1.29-2.91]) and gases and fumes (relative risk, 1.53 [0.99-2.36]), which was not modified by smoking. CONCLUSION: Occupational exposures to dusts, gases, and fumes occurring during the 1990s are associated with incidence of chronic bronchitis, although these did not impair lung function in a population of relatively young age.
Occupational exposure to antineoplastic cytostatic drugs has been recognized as a potential health hazard since the seventies. Safety guidelines and recommendations have been published in several countries in order to improve operating procedures and keep exposure levels as low as possible. Nevertheless, contamination still occurs. With a view to preventing exposure, standardized authorized methods and a mandatory monitoring system appear to be an essential prerequisite. First of all, reliable analytical methods are necessary, and a wide number of drugs should be monitored, on the basis of the continual change in the treatment protocols. In fact, most of the methods available in the literature were not properly validated, and a lack of details concerning quality assurance is clearly observed. When assessing analytical methods applied for routine testing, validation studies are of utmost importance. Not only performance parameters, such as sensitivity, specificity, LOD and LLQ, should therefore be determined, but also the uncertainty of measurement, which gives a measure of the confidence that can be placed on the results.
Occupational exposure to pesticides in agriculture and public health applications may cause acute and long-term health effects. Prevention of adverse effects in the users requires actions to be undertaken in the pre-marketing and post-marketing phase of these products. The pre-marketing preventive actions are primary responsibility of industry and the public administration. Admission of pesticide use (registration) is carried out by considering the toxicological properties of each pesticide (hazard identification), determining the dose-response relationship (NOEL identification), assessing or predicting the exposure level in the various scenarios of their use, and characterising the risk. The decision about admission takes into consideration the balance between risks and benefits. The post-marketing preventive activities consist of the promotion of a proper risk management at the workplace. Such a management includes the risk assessment of the specific conditions of use, the adoption of proper work practices, and the health surveillance of the workers. Each country should develop an adequate National Plan for Prevention of Pesticide Risk which allocates different roles and tasks at the central, regional and local level.
The influence of occupational exposures on total mortality and respiratory mortality and morbidity was examined, employing a population specific Job Exposure Matrix (JEM). Moreover, the relationship between time-related variables of exposure to dust and chronic nonspecific lung disease (CNSLD) incidence was analysed, using time since first exposure and duration of exposure. Occupational exposures in the Zutphen cohort were assessed by application of a JEM, arbitrarily considering jobs as exposed when at least 10% of men who had held the job of interest reported an exposure to one or more from a list of 27 chemical agents. None of the exposures was related to mortality due to CNSLD, although results were influenced by the healthy-worker effect and low mortality rates. Exposure to wood dust and a high probability of exposure to dust were associated with total mortality. Exposures to dust and solvents were statistically significantly related to CNSLD incidence. An exposure-response relationship was found for the probability of exposure to dust with CNSLD incidence. Time-related estimates of exposure to dust based on work history were negatively related to CNSLD incidence. The results suggest the presence of a healthy-worker effect, in a general population study, resulting in an underestimation of the relationship between occupational exposures and respiratory diseases based on the evidence published so far. The use of the full work history to determine exposure to dust leads to stronger relationships with CNSLD incidence, compared to conventional analyses using exposure at the start of follow-up.
The Occupational Safety and Health Administration (OSHA) has regulated occupational exposure to asbestos since 1971. Since issuing its first asbestos standard, OSHA has modified it several times in response to new information about the health risk of exposure and concern expressed by workers and public health groups. As each modification has reduced worker exposure and disease risk, each also has introduced new concepts including emphasis on ancillary provisions in standards regulating occupational exposure to toxic substances to enhance worker health; medical removal protection; two attempts at emergency temporary standards; use of historical and objective exposure data to assess worker exposure; the need to eliminate significant risk of disease posed by asbestos; and the presumption of hazard in absence of exposure information. These and other advances have affected all subsequent OSHA standards aimed at reducing occupational exposure to toxic substances.