Hearing conservation in the primary aluminium industry.

BACKGROUND: Noise-induced hearing loss has been an intractable problem for heavy industry. AIMS: To report our experience in reducing the incidence of age-corrected confirmed 10 dB hearing shifts (averaged over 2, 3 and 4 kHz) in employees in the primary aluminium industry in Australia over the period 2006-13. METHODS: We analysed annual audiometric data to determine the number of permanent hearing shifts that occurred in employees in two bauxite mines, three alumina refineries and two aluminium smelters. Annual hearing shift rates were calculated based on the number of employees tested per year. Hearing conservation initiatives undertaken during the study period are described. An assessment of similar exposure group noise exposures was also undertaken to determine the magnitude of noise exposure reduction during the study period. RESULTS: Across all operations, hearing shift rates declined from 5.5% per year in 2006 to 1.3% per year in 2013 (P < 0.001). The decline in shift rates was greater in mines and refineries, where baseline shift rates were higher, than in smelter workers. Modest reductions in noise exposure occurred during the study period. CONCLUSIONS: We observed a substantial decline in hearing shift rates during the study period. We describe the hearing conservation initiatives that were collectively associated with this decline. We suspect these initiatives could be deployed relatively easily and at modest cost in other industries with noise-exposed employees.

Prevalence of beryllium sensitization among aluminium smelter workers.

BACKGROUND: Beryllium exposure occurs in aluminium smelters from natural contamination of bauxite, the principal source of aluminium. AIMS: To characterize beryllium exposure in aluminium smelters and determine the prevalence rate of beryllium sensitization (BeS) among aluminium smelter workers. METHODS: A population of 3185 workers from nine aluminium smelters owned by four different aluminium-producing companies were determined to have significant beryllium exposure. Of these, 1932 workers participated in medical surveillance programmes that included the serum beryllium lymphocyte proliferation test (BeLPT), confirmation of sensitization by at least two abnormal BeLPT test results and further evaluation for chronic beryllium disease in workers with BeS. RESULTS: Personal beryllium samples obtained from the nine aluminium smelters showed a range of <0.01-13.00 µg/m(3) time-weighted average with an arithmetic mean of 0.25 µg/m(3) and geometric mean of 0.06 µg/m(3). Nine workers were diagnosed with BeS (prevalence rate of 0.47%, 95% confidence interval = 0.21-0.88%). CONCLUSIONS: BeS can occur in aluminium smelter workers through natural beryllium contamination of the bauxite and further concentration during the refining and smelting processes. Exposure levels to beryllium observed in aluminium smelters are similar to those seen in other industries that utilize beryllium. However, compared with beryllium-exposed workers in other industries, the rate of BeS among aluminium smelter workers appears lower. This lower observed rate may be related to a more soluble form of beryllium found in the aluminium smelting work environment as well as the consistent use of respiratory protection.

Organic solvent exposure and hearing loss in a cohort of aluminium workers.

OBJECTIVES: Organic solvent exposure has been shown to cause hearing loss in animals and humans. Less is known about the risk of hearing loss due to solvent exposures typically found in US industry. The authors performed a retrospective cohort study to examine the relationship between solvent exposure and hearing loss in US aluminium industry workers. METHODS: A cohort of 1319 workers aged 35 years or less at inception was followed for 5 years. Linkage of employment, industrial hygiene and audiometric surveillance records allowed for estimation of noise and solvent exposures and hearing loss rates over the study period. Study subjects were classified as "solvent exposed" or not, on the basis of industrial hygiene records linked with individual job histories. High frequency hearing loss was modelled as both a continuous and a dichotomous outcome. RESULTS: Typical solvent exposures involved mixtures of xylene, toluene and/or methyl ethyl ketone (MEK). Recorded solvent exposure levels varied widely both within and between jobs. In a multivariate logistic model, risk factors for high frequency hearing loss included age (OR = 1.06, p = 0.004), hunting or shooting (OR = 1.35, p = 0.049), noisy hobbies (OR = 1.74, p = 0.01), baseline hearing level (OR = 1.04, p<0.001) and solvent exposure (OR = 1.87, p = 0.004). A multivariate linear regression analysis similarly found significant associations between high frequency hearing loss and age (p<0.001), hunting or shooting (p<0.001), noisy hobbies (p = 0.03), solvent exposure (p<0.001) and baseline hearing (p = 0.03). CONCLUSION: These results suggest that occupational exposure to organic solvent mixtures is a risk factor for high frequency hearing loss, although the data do not allow conclusions about dose-response relationships. Industries with solvent-exposed workers should include such workers in hearing conservation programs.

Cross-national comparisons of increasing suicidal mortality rates for Koreans in the Republic of Korea and Korean Americans in the USA, 2003-2012.

AIMS: Korea has the highest suicide rate of developed countries, two times higher than the USA. Suicide trends among Koreans Americans living in the USA during the same period have not yet been described. We report suicide mortality rates and trends for four groups: (1) Korean Americans, (2) non-Hispanic White (NHW) Americans, (3) selected Asian American subgroups and (4) Koreans living in the Republic of Korea. METHODS: We used US national (n = 18 113 585) and World Health Organization (WHO) (n = 232 919 253) mortality records for Korea from 2003 to 2012 to calculate suicide rates, all expressed per 100 000 persons. We assessed temporal trends and differences in age, gender and race/ethnicity using binomial regression. RESULTS: Suicide rates are highest in Koreans living in the Republic of Korea (32.4 for men and 14.8 for women). Suicide rates in Korean Americans (13.9 for men and 6.5 for women) have nearly doubled from 2003 to 2012 and exceed rates for all other Asian American subgroups (5.4-10.7 for men and 1.6-4.2 for women). Suicide rates among NHWs (21.0 for men and 5.6 for women) remain high. Among elders, suicide in Korean Americans (32.9 for men and 15.4 for women) is the highest of all examined racial/ethnic groups in the USA. CONCLUSIONS: Suicide in Korean Americans is higher than for other Asian Americans and follows temporal patterns more similar to Korea than the USA. Interventions to prevent suicide in Korean American populations, particularly among the elderly, are needed.

Do ambient noise exposure levels predict hearing loss in a modern industrial cohort?

BACKGROUND: Much of what is known about the exposure-response relationship between occupational noise exposures and hearing loss comes from cross-sectional studies conducted before the widespread implementation of workplace hearing conservation programmes. Little is known about the current relationship of ambient noise exposure measurements to hearing loss risk. AIM: To examine the relationship between rates of high frequency hearing loss and measured levels of noise exposure in a modern industrial workforce. METHODS: Ten-year hearing loss rates were determined for 6217 employees of an aluminium manufacturing company. Industrial hygiene and human resources records allowed for reconstruction of individual noise exposures. Hearing loss rates were compared to ANSI 3.44 predictions based on age and noise exposure. Associations between hearing loss, noise exposure, and covariate risk factors were assessed using multivariate regression. RESULTS: Workers in higher ambient noise jobs tended to experience less high frequency hearing loss than co-workers exposed at lower noise levels. This trend was also seen in stratified analyses of white males and non-hunters. At higher noise exposure levels, the magnitude of hearing loss was less than predicted by ANSI 3.44 formulae. There was no indication that a healthy worker effect could explain these findings. The majority of 10 dB standard threshold shifts (STS) occurred in workers whose calculated ambient noise exposures were less than or equal to 85 dBA. CONCLUSIONS: In this modern industrial cohort, hearing conservation efforts appear to be reducing hearing loss rates, especially at higher ambient noise levels. This could be related to differential use of hearing protection. The greatest burden of preventable occupational hearing loss was found in workers whose noise exposure averaged 85 dBA or less. To further reduce rates of occupational hearing loss, hearing conservation programmes may require innovative approaches targeting workers with noise exposures close to 85 dBA.

Risk factors for lung cancer and for intervention effects in CARET, the Beta-Carotene and Retinol Efficacy Trial.

BACKGROUND: Evidence has accumulated from observational studies that people eating more fruits and vegetables, which are rich in beta-carotene (a violet to yellow plant pigment that acts as an antioxidant and can be converted to vitamin A by enzymes in the intestinal wall and liver) and retinol (an alcohol chemical form of vitamin A), and people having higher serum beta-carotene concentrations had lower rates of lung cancer. The Beta-Carotene and Retinol Efficacy Trial (CARET) tested the combination of 30 mg beta-carotene and 25,000 IU retinyl palmitate (vitamin A) taken daily against placebo in 18314 men and women at high risk of developing lung cancer. The CARET intervention was stopped 21 months early because of clear evidence of no benefit and substantial evidence of possible harm; there were 28% more lung cancers and 17% more deaths in the active intervention group (active = the daily combination of 30 mg beta-carotene and 25,000 IU retinyl palmitate). Promptly after the January 18, 1996, announcement that the CARET active intervention had been stopped, we published preliminary findings from CARET regarding cancer, heart disease, and total mortality. PURPOSE: We present for the first time results based on the pre-specified analytic method, details about risk factors for lung cancer, and analyses of subgroups and of factors that possibly influence response to the intervention. METHODS: CARET was a randomized, double-blinded, placebo-controlled chemoprevention trial, initiated with a pilot phase and then expanded 10-fold at six study centers. Cigarette smoking history and status and alcohol intake were assessed through participant self-report. Serum was collected from the participants at base line and periodically after randomization and was analyzed for beta-carotene concentration. An Endpoints Review Committee evaluated endpoint reports, including pathologic review of tissue specimens. The primary analysis is a stratified logrank test for intervention arm differences in lung cancer incidence, with weighting linearly to hypothesized full effect at 24 months after randomization. Relative risks (RRs) were estimated by use of Cox regression models; tests were performed for quantitative and qualitative interactions between the intervention and smoking status or alcohol intake. O'Brien-Fleming boundaries were used for stopping criteria at interim analyses. Statistical significance was set at the .05 alpha value, and all P values were derived from two-sided statistical tests. RESULTS: According to CARET's pre-specified analysis, there was an RR of 1.36 (95% confidence interval [CI] = 1.07-1.73; P = .01) for weighted lung cancer incidence for the active intervention group compared with the placebo group, and RR = 1.59 (95% CI = 1.13-2.23; P = .01) for weighted lung cancer mortality. All subgroups, except former smokers, had a point estimate of RR of 1.10 or greater for lung cancer. There are suggestions of associations of the excess lung cancer incidence with the highest quartile of alcohol intake (RR = 1.99; 95% CI = 1.28-3.09; test for heterogeneity of RR among quartiles of alcohol intake has P = .01, unadjusted for multiple comparisons) and with large-cell histology (RR = 1.89; 95% CI = 1.09-3.26; test for heterogeneity among histologic categories has P = .35), but not with base-line serum beta-carotene concentrations. CONCLUSIONS: CARET participants receiving the combination of beta-carotene and vitamin A had no chemopreventive benefit and had excess lung cancer incidence and mortality. The results are highly consistent with those found for beta-carotene in the Alpha-Tocopherol Beta-Carotene Cancer Prevention Study in 29133 male smokers in Finland.

The beta-carotene and retinol efficacy trial (CARET) for chemoprevention of lung cancer in high risk populations: smokers and asbestos-exposed workers.

CARET is a multicenter, two-armed, double-masked randomized chemoprevention trial in Seattle, Portland, San Francisco, Baltimore, Connecticut, and Irvine, to test whether oral administration of beta-carotene (30 mg/day) plus retinyl palmitate (25,000 IU/day) can decrease the incidence of lung cancer in high risk populations, namely, heavy smokers and asbestos-exposed workers. The intervention combines the antioxidant action of beta-carotene and the tumor suppressor mechanism of vitamin A. As of April 30, 1993, CARET had randomized 1,845 participants in the 1985-1988 pilot phase plus 13,260 "efficacy" participants since 1989; of these, 4,000 are asbestos-exposed males and 11,105 are smokers and former smokers (44% female). Accrual is complete everywhere except Irvine, which was the last center added (1991), and the safety profile of the regimen to date has been excellent. With 14,420 smokers, 4,010 asbestos-exposed participants, and 114,100 person-years through February 1998, we expect CARET to be capable of detecting a 23% reduction in lung cancer incidence in the two populations combined and 27, 49, 32, and 35% reductions in the smokers, female smokers, male smokers, and asbestos-exposed subgroups, respectively. CARET is highly complementary to the alpha-tocopherol-beta-carotene study in Finland and the Harvard Physicians Health Study (beta-carotene alone) in the National Cancer Institute portfolio of major cancer chemoprevention trials.

Changes in cholesterol and triglyceride concentrations in the Vanguard population of the Carotene and Retinol Efficacy Trial (CARET).

BACKGROUND: The Beta-Carotene and Retinol Efficacy Trial (CARET) was terminated 21 months ahead of schedule due to an excess of lung cancers. Deaths from cardiovascular disease also increased (relative risk=1.26 (95% confidence interval (CI) 0.99-1.61)) in the group assigned to a combination of 30 mg beta-carotene and 25 000 IU retinyl palmitate (vitamin A) daily. The basis for increased cardiovascular mortality is unexplained. DESIGN: We analyzed data on serum lipids, available for 1474 CARET Vanguard participants who were enrolled in the two CARET pilot studies and transitioned to the Vanguard study. Total cholesterol and triglycerides were measured 2 months prior to, 4 and 12 months following randomization, and annually thereafter for up to 7 y. INTERVENTION: In the asbestos-exposed pilot (N = 816), participants were assigned to beta-carotene and retinol or to placebo; in the smokers pilot (N = 1029), participants were assigned to beta-carotene, retinol, a combination, or placebo. RESULTS: Serum cholesterol showed a decline over time in both arms; serum triglycerides had a continuous decline over time in the placebo arm, but an initial increase that persisted in the active arm. Both serum cholesterol concentrations (P < 0.0003) and serum triglycerides (P < 0.0001) were significantly higher in the participants receiving vitamin A and/or a combination of vitamin A and beta-carotene (n = 863) as compared to the placebo group (n = 611). Those in this active intervention group had an average cholesterol concentration 5.3 mg/dl (0.137 mmol/l) higher than those in the placebo arm. CONCLUSION: The differences in cholesterol and triglyceride concentrations between the groups following randomization may account in part for the unexpected excess in cardiovascular deaths seen in the active intervention arm of CARET.

Occupational medicine. A new focus for general internal medicine.

In the past two decades, occupational medicine has advanced from a formerly clinical discipline to one focused on epidemiology and toxicology. However, because efforts to prevent occupational disease by concerted application of industrial hygiene have not eliminated the problem, there remains a strong need for clinical interventions. Appropriate interventions could result in a further substantial reduction in the morbidity and mortality of work-connected illness. Unfortunately, neither adequate training nor the necessary scientific foundation for clinical decision making presently exist. Studies are needed to characterize the modern spectra and natural histories of virtually all recognized occupational diseases and to evaluate the efficacy of available therapeutic strategies. Sections of general internal medicine potentially offer an ideal academic setting to address these educational and scientific deficiencies.

The challenge of teaching occupational and environmental medicine in internal medicine residencies.

Using a mailed survey questionnaire directed toward division chiefs of general internal medicine, we have confirmed that despite increased interest among faculty, few medical residents currently receive required or elective training in occupational medicine. However, recent changes in societal perceptions about environmental risks, corporate health care practices, and medical reimbursement patterns favoring provision by hospitals of contractual outpatient services to healthy workers all portend expanded involvement of residents in certain occupational medicine activities in the future, in response to economic pressures on both consumers and providers. These same forces may, unfortunately, undermine the scientific and ethical quality of such training experiences, compared with emerging, more academically motivated approaches. The implications of these prospects are analyzed in the hope that a proper balance can ultimately be struck between economic and academic imperatives.

Spectrum of occupational disease in an academic hospital-based referral center in Connecticut from 1979 to 1987.

The inability to characterize the extent of occupational disease in the United States limits clinical diagnosis and public health interventions. We present an 8-year (1979 to 1987) experience with clinic-based reporting in Connecticut. Altogether, 3566 cases were sequentially coded for demographics, diagnoses, workplace identification, and exposures at two academic occupational medicine clinics. The lungs were the principal organs of diagnosed effect, with asbestos-related disorders predominating, whereas the urinary tract, endocrine organs, and cardiovascular systems were rarely involved. Of all diseases, 64.8% were diagnosed as chronic and irreversible. Three common disorders, lead intoxication (acute and chronic), asbestosis, and occupational asthma were selected for illustration. Patients with lead poisoning and asbestosis, although collectively numerous (40 and 504, respectively), came from a small number of worksites and industries. Occupational asthma was more variable: 141 diagnosed cases came from 56 different trades and industries and were caused by 28 recognized agents. While we recognize that clinic-based reporting suffers from obvious problems with referral bias and misclassification, our experience shows that it provides an important index of disease burden. Our data document the effects of legislation and litigation on lead poisoning and asbestosis, and correspondingly helps characterize diseases that will respond to broad intervention. On the other hand, occupational asthma is more pervasive and would require a more specialized, partially clinical approach.

Depressed thyroid indexes associated with occupational exposure to inorganic lead.

The finding of low values for serum thyroxine and estimated free thyroxine in seven of 12 workers referred because of elevated blood lead levels (greater than 40 mg/L) prompted further investigation. In a cross-sectional study of workers at a small foundry, both measurements were found to regress negatively with blood lead level. In 12 of 47 subjects, both indexes were in the hypothyroid range. Serum thyrotropin and triiodothyronine levels in patients and study subjects with low indexes were all normal. Physical examinations failed to demonstrate the classic features of hypothyroidism. These data are compatible with a central depression of the thyroid axis or an alteration in thyroxine metabolism or binding to proteins. Irrespective of mechanism, the association between low thyroid indexes and elevated lead levels merits attention because of the large number of workers exposed to lead and the similarities between the clinical features of adult lead poisoning and hypothyroidism.

Organic affective illness associated with lead intoxication.

Psychiatrists treating patients with depression or nonspecific somatic complaints seldom think of lead intoxication as a possible cause. Because occupational exposure to lead is so common, these disturbances may often be associated with lead intoxication. To facilitate earlier clinical recognition and proper treatment among the many individuals at risk, the authors describe four cases of organic affective disturbance associated with lead intoxication, review the neuropsychiatric disturbances that have been reported with chronic exposure to lead, and report the results of their experience evaluating the psychiatric aspects of lead intoxication among individuals exposed in their work.

Occupation-induced posttraumatic stress disorders.

The authors describe a variant of posttraumatic stress disorder that presents as a somatoform disorder. Applying clearly specified diagnostic criteria, they found that seven of 21 patients who were severely disabled by medically unexplained symptoms following occupational exposure to toxic substances had atypical posttraumatic stress disorder, while three patients had typical posttraumatic stress disorder and the remainder suffered from somatoform disorders. Analysis of these cases revealed specific exposure factors and personality characteristics that favor the development of atypical posttraumatic stress disorder. The authors discuss the theoretical, clinical, and therapeutic advantages of this diagnosis.

Dietary vitamin A and prevalence of bronchial metaplasia in asbestos-exposed workers.

The purpose of this investigation was to examine the association between dietary intake of vitamin A in the form of retinol and provitamin A carotenoids and the prevalence of bronchial squamous metaplasia in a sample of asbestos workers from an industrial clinic. Bronchial biopsies were obtained from 49 asbestos workers. Pulmonary function testing was done and in-person interviews were conducted to estimate dietary intake of retinol and provitamin A carotenoids, tobacco exposure, and asbestos exposure. Results indicated that workers with metaplasia reported consuming a significantly lower intake of total vitamin A [2000 retinol equivalents (RE)/d] than did subjects without metaplasia (2710 RE/d, P = 0.02). Logistic regression analyses showed that higher intakes of retinol [odds ratio (OR): 0.31; 95% CI: 0.04, 2.44], provitamin A carotenoids (OR: 0.31; 95% CI: 0.03, 2.84), and total vitamin A (OR: 0.29; 95% CI: 0.03, 2.49) were associated with a nonsignificant reduction in the OR for metaplasia (highest quartile compared with lowest quartile, adjusted ORs). Current smoking (OR: 5.25; 95% CI: 0.50, 55.1) and former smoking (OR: 2.95; 95% CI: 0.31, 28.1) were associated with a nonsignificant increase in the OR for bronchial metaplasia compared with never smoking. Greater airway obstruction [decreased forced expiratory volume in 1 s (FEV1)/forced vital capacity (FVC)] was associated with an increased OR for metaplasia (OR: 2.86; 95% CI: 1.09, 7.69). These results suggest that a higher (ie, above the median) intake of vitamin A from foods decreases the risk of bronchial metaplasia in workers occupationally exposed to asbestos.

Effect of supplementation with beta-carotene and vitamin A on lung nutrient levels.

The Carotene and Retinol Efficacy Trial (CARET), a randomized, placebo-controlled lung cancer chemoprevention trial of 30 mg of beta-carotene and 25,000 IU of retinyl palmitate, was prematurely terminated when a 46% excess lung cancer mortality was found in subjects on the active arm. Before the CARET intervention ended, 21 men were recruited to participate in a 6-month biomarker study using the same intervention as CARET that determined the effect of this supplementation on lung nutrient levels. Plasma and bronchoalveolar lavage (BAL) cell nutrient levels were measured before and after the intervention. The group in the active arm (n = 10) had plasma carotene level increases of over 10-fold, with a small increase in plasma retinol levels BAL cell levels of beta-carotene in the active group also increased 10-fold, from 4.5 to 46.3 pmol/10(6) cells (P = 0.0008), with no change in BAL cell retinol levels. Surgically obtained lung tissue from three CARET subjects in the active arm showed elevated carotene lung tissue levels but no increase in lung retinol levels compared to a group of surgical controls. Combined with our previous work showing a strong correlation between BAL and lung tissue nutrient levels, these findings suggest that supplementation with beta-carotene and vitamin A results in increased lung tissue as well as BAL cell levels of beta-carotene, with little change in lung retinol.

Effect of long-term beta-carotene and vitamin A on serum cholesterol and triglyceride levels among participants in the Carotene and Retinol Efficacy Trial (CARET)

OBJECTIVE: The Carotene and Retinol Efficacy Lung Cancer Chemoprevention Trial (CARET) ended prematurely due to the unexpected findings that the active treatment group on the combination of 30 mg beta-carotene and 25,000 IU retinyl palmitate had a 46% increased lung cancer mortality and a 26% increased cardiovascular mortality compared with placebo. This study was designed when the CARET intervention was halted to evaluate the effects of long-term supplementation with beta-carotene and retinol on serum triglyceride and cholesterol levels, in an attempt to explore possible explanations for the CARET result. METHODS: Serum triglyceride levels, and total, high-density lipoprotein (HDL), and low-density lipoprotein (LDL) cholesterol levels were determined in a subgroup of 52 CARET participants. Baseline and mid-trial levels were available on 23 participants on placebo and 29 on active treatment who were then serially followed for 10 months after trial termination. RESULTS: Triglyceride, and total, HDL and LDL cholesterol levels were similar in the two groups at baseline. After a mean of 5 years on the intervention there was a small nonsignificant increase in serum triglyceride levels in the active group, but no difference in total, HDL, or LDL cholesterol levels. After stopping the intervention there was a decrease in triglyceride levels in the active intervention group, and no change in the other parameters. CONCLUSION: Based on a small convenience sample, CARET participants in the active treatment arm had a small nonsignificant increase in serum triglyceride levels while on the intervention, and a decrease in serum triglyceride levels after the intervention was discontinued. No significant changes in total or HDL cholesterol were noted. These results argue against a major contribution of treatment-induced changes in serum lipid and lipoprotein levels to the increased cardiovascular mortality in the active treatment group.

Effect of long-term beta-carotene and vitamin A on serum cholesterol and triglyceride levels among participants in the Carotene and Retinol Efficacy Trial (CARET)

OBJECTIVE: The Carotene and Retinol Efficacy Lung Cancer Chemoprevention Trial (CARET) ended prematurely due to the unexpected findings that the active treatment group on the combination of 30 mg beta-carotene and 25,000 IU retinyl palmitate had a 46% increased lung cancer mortality and a 26% increased cardiovascular mortality compared with placebo. This study was designed when the CARET intervention was halted to evaluate the effects of long-term supplementation with beta-carotene and retinol on serum triglyceride and cholesterol levels, in an attempt to explore possible explanations for the CARET result. METHODS: Serum triglyceride levels, and total, high-density lipoprotein (HDL), and low-density lipoprotein (LDL) cholesterol levels were determined in a subgroup of 52 CARET participants. Baseline and mid-trial levels were available on 23 participants on placebo and 29 on active treatment who were then serially followed for 10 months after trial termination. RESULTS: Triglyceride, and total, HDL and LDL cholesterol levels were similar in the two groups at baseline. After a mean of 5 years on the intervention there was a small nonsignificant increase in serum triglyceride levels in the active group, but no difference in total, HDL, or LDL cholesterol levels. After stopping the intervention there was a decrease in triglyceride levels in the active intervention group, and no change in the other parameters. CONCLUSION: Based on a small convenience sample, CARET participants in the active treatment arm had a small nonsignificant increase in serum triglyceride levels while on the intervention, and a decrease in serum triglyceride levels after the intervention was discontinued. No significant changes in total or HDL cholesterol were noted. These results argue against a major contribution of treatment-induced changes in serum lipid and lipoprotein levels to the increased cardiovascular mortality in the active treatment group.

Screening for lead poisoning in an urban pediatric clinic using samples obtained by fingerstick.

OBJECTIVE: To assess the false positive rate of blood lead (BPb) determinations on samples obtained by fingerstick from children screened in an urban clinic. METHOD: From a single fingerstick (N = 1573), blood was collected in a capillary tube for determining lead concentration (CPb) by graphite furnace and an additional sample was absorbed onto a filter paper for determining lead concentration (FPb) by atomic absorption spectrophotometry with Delves cup. Zinc protoporphyrin (ZPP) was measured immediately and a confirmatory venous lead (VPb) specimen was obtained at the same visit if the ZPP was > or = 35 micrograms/dL (0.6 mumol/L); children with either a CPb or FPb > or = 15 micrograms/dL (0.7 mumol/L) were later recalled for determining VPb. RESULTS: For the 172 children who had a VPb on the same day as the screening tests, the false positive rates (95% confidence intervals) at a lead threshold of 15 micrograms/dL (0.7 mumol/L) were: CPb, 13.5% (6.7-20.3); FPb, 19.1% (11.8-26.4). Analyses using all 679 screens with a paired venous specimen (mean delay between screen and venous testing = 30 days) yielded much higher false positive rates (CPb, 31.3%; FPb, 46.0%). CONCLUSIONS: Screening for lead poisoning is feasible within an urban pediatric clinic by direct measurement of lead concentration in blood samples obtained by fingerstick. The false positive rate that can be obtained is acceptable given the precision of measuring BPb concentration. Practitioners using a staged screening protocol may incorrectly attribute a higher false positive rate to the screening tests, when much of the error may be due to the temporal variability of BPb resulting from both biologic variability in BPb concentration and intermittent exposures.

Association between neutrophil concentration in bronchoalveolar lavage fluid and recent losses in diffusing capacity in men formerly exposed to asbestos.

It has been observed widely that some individuals exposed to asbestos will experience continued losses of lung function after asbestos exposure ceases. Unfortunately, there are few data on factors that determine clinical course, limiting the clinician's ability to determine prognosis in an individual case and restricting the possibility for testing or targeting any potential intervention to alter the course among the millions at risk. In an attempt to address this question, we studied a volunteer population of 50 such men from among a stable, heterogeneous population of asbestos-exposed workers who had been continuously followed in our occupational medicine clinics for up to 12 years (mean, 6.3 years); most had some clinical or roentgenographic sign of asbestos effect, pleural or parenchymal. Each subject was reexamined clinically, functionally, and roentgenographically. Asbestos and tobacco exposure histories were carefully reviewed with the subjects and quantified based on these reports and available data regarding the various work environments from which they came. Subsequently, each underwent a bronchoalveolar lavage to assess cellularity and levels of various proteins. The levels of risk factors, clinical findings, and biologic parameters from lavage were examined for their relationship to serial changes in lung function during the period over which they had been previously followed. Results of the study demonstrate that serial changes in lung function were not closely related to level or length of prior exposure, smoking behavior, chest roentgenographic findings, or lung volumes. Progressive loss of diffusing capacity for carbon monoxide (Dco) was significantly associated with two factors: level of neutrophil concentration in lavage fluid (0.043 +/- 0.016 ml/min/mm Hg/yr drop for each 0.1 x 10(4) neutrophils per milliliter, p = 0.02) and the level of Dco itself (0.17 +/- 0.07 ml/min/mm Hg/yr drop for each 10 percent decrease in percent Dco predicted, p = 0.01). The relationship with neutrophil concentration was statistically independent of the association with Dco itself and stronger; it persisted when loss of Dco was adjusted for baseline value. Lung volume changes were not associated with any predictor variables, alone or in combination. We conclude that the presence of neutrophils in bronchoalveolar lavage fluid is associated with recent disease progression that may have implications in studies of the mechanisms of asbestos-associated disease and in clinical treatment of patients at risk.