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Biomedical subjects

D C Christiani

Publications and source records attributed to D C Christiani.

At least 127 records · Page 7Linked to original sources
PubMed1996

Medical surveillance for ethylene oxide exposure: practices and clinical findings in Massachusetts hospitals.

The medical surveillance requirements of the Occupational Safety and Health Administration's (OSHA) ethylene oxide (EtO) standard became effective in 1985. However, little is known about the nature of the response of EtO users to this regulatory requirement. In an effort to begin to understand this, we conducted a survey of EtO health and safety in Massachusetts hospitals (n = 92). We determined the cumulative incidence of provision of EtO medical surveillance, the characteristics of the surveillance interventions provided, and the clinical findings of EtO medical surveillance efforts in Massachusetts hospitals. From 1985 to 1993, medical surveillance for EtO exposure was provided one or more times in 62% of EtO-using hospitals. Sixty-five percent of EtO medical surveillance providers reported performance of all five medical surveillance procedures required by OSHA's EtO standard. Medical surveillance provider certification in occupational medicine or nursing, and a greater extent of coverage of written medical surveillance policies, were related to higher likelihoods of fulfillment of OSHA-required procedures. Twenty-seven percent of medical surveillance providers reported detection of EtO-related symptoms or conditions, ranging from mucous membrane irritation to peripheral neuropathy. These findings reveal wide-spread implementation of OSHA-mandated EtO medical surveillance, with concomitant incomplete fulfillment of OSHA-specified procedures. From the provider-based survey, we estimate that one or more workers at 19% of EtO-using Massachusetts hospitals have experienced EtO-related health effects.

Adult↗
PubMed1996

Epidemiology of hazardous materials responses by Massachusetts district HAZMAT teams.

Hazardous materials releases can cause substantial morbidity and mortality, but very few studies have systemically investigated them. We analyzed responses by Massachusetts' six district hazardous materials (HAZMAT) teams from the time of their inception through February 1994. Spills, leaks, and other escapes of materials caused or contributed to 67 of 85 (79%) incidents. Transportation-related accidents accounted for 13 of 83 (16%), whereas the remainder of the releases occurred at fixed facilities. The chemicals most frequently involved were various hydrocarbons and corrosive materials. Most incidents (60 of 85 [70%]) had no reported injuries. Civilians were injured in 18 of 85 (21%) incidents; regular fire fighter and/or police were injured in eight of 85 (9%) incidents; and HAZMAT team members in one of 85 incidents (1%). Systematic study is needed to identify preventable causes of HAZMAT responses as well as ideas for better control of secondary health effects.

Accidents, Occupational↗
PubMed1996

T cell activation in a murine model of asthma.

To determine the mechanisms by which inhaled antigens produce pulmonary inflammation and bronchial hyperreactivity, we have developed a murine model of asthma. BALB/c mice are sensitized and challenged with ovalbumin (OVA). Compared with mice treated with phosphate-buffered saline (PBS), OVA-treated mice developed increased lung resistance, decreased dynamic compliance, and greater methacholine reactivity. Bronchoalveolar lavage fluid revealed significant increases in the proportion of neutrophils and eosinophils. Tissue sections of OVA-treated mice demonstrated goblet cell metaplasia and focal perivascular and peribronchial infiltrates composed of lymphocytes, neutrophils, and eosinophils. Analysis of thoracic lymphocytes via flow cytometry revealed an expansion of both CD4+ and B cell populations, with increased expression of interleukin-2 receptor on CD4+ T cells, indicated increased activation. There was also increased expression of CD44 on CD4+ and CD8+ lymphocytes, suggesting an expansion of the local memory cell population. These findings support the hypothesis that activation of T lymphocytes mediates allergic pulmonary inflammation and bronchial reactivity in asthma.

Animals↗
PubMed1996

A regression approach to the analysis of serial peak flow among fuel oil ash exposed workers.

We investigated the association between exposure to fuel oil ash and acute airway obstruction in 31 boilermakers and 31 utility workers during the overhaul of a large oil-fired boiler. Air flow was assessed with self-recorded serial peak expiratory flow rate measurements (PEFR) using a mini-Wright meter. Exposure to thoracic particulates with an aerodynamic diameter of 10 gm or smaller (PM10) was assessed using personal sampling devices and detailed work diaries. All subjects were male, with an average age of 43 yr, and an average of 18 yr at their current trade. Average PM10 exposure on work days was 2.75 mg/m3 for boilermakers and 0.57 mg/m3 for utility workers. Three daily PEFR measurements (start-of-shift, end-of-shift, and bed-time) were analyzed simultaneously, using Huber linear regression. After adjustment for job title, welder status, age, height, smoking, and weld-years, for each mg/m3 increase in PM10, the estimated decline in PEFR was 13.2 L/min (p = 0.008) for end-of-shift, 9.9 L/min (p = 0.045) for bed-time, and 6.6 L/min (p = 0.26) for start-of-shift of the following day. This decline of the exposure effect over the 24-h period that follows was statistically significant (p = 0.004). No other factors were found to significantly modify the effect of exposure. Our results suggest that occupational exposure to fuel oil ash is associated with significant acute decrements in peak flow.

Adult↗
PubMed1996

Utilization of biomarker data for clinical and environmental intervention.

Of the 189 air toxics listed in the Clean Air Act, a substantial number are important in potentially causing adverse health effects in several organ systems. Although the major health effects are manifested as respiratory diseases, especially airways disease, these agents may cause cancer and premature mortality, probably from cardiopulmonary disease. Validated biologic markers may be useful in identifying early effects to improve our understanding of exposure-response relationships and clarify susceptibility. However, the knowledge obtained from epidemiologic studies utilizing these new molecular tools will reduce morbidity and mortality from air toxics only when they can be applied effectively in the prevention and control of disease. Intervention strategies using these markers can be used to identify etiologic factors and assess the effectiveness of exposure reduction, and, in some instances, chemoprevention. This paper illustrates examples of these intervention strategies and reviews the current strengths and limitations of environmental molecular epidemiology in controlling disease caused by air toxics.

Air Pollutants↗
PubMed1996

Cytochrome P450 CYP1A1 MspI polymorphism and lung cancer susceptibility.

We conducted a case-control study of 207 lung cancer patients and 283 controls to estimate the association of the MspI polymorphism in the cytochrome P450 CYP1A1 gene with lung cancer. The analysis of the CYP1A1 gene polymorphism was performed by RFLP analysis of PCR-amplified DNA. The association of the CYP1A1 polymorphism with lung cancer was assessed by logistic regression using the generalized additive modeling technique to adjust for race, education, smoking status, pack years, time since quitting smoking, asbestos exposures, and family cancer history. The frequencies of the MspI homozygote and heterozygote variant genotypes of CYP1A1 were 1% and 17%, respectively, in both lung cancer patients and controls. A significant association was found between the combined heterozygous and homozygous MspI variant of the CYP1A1 gene and lung cancer; the estimated odds ratio was 2.08 (95% confidence interval, 1.15-3.73). The association remained significant when we excluded the homozygous MspI variant individuals, the non-Caucasians, or the long-time tobacco quitters, and it was not modified by gender or cumulative cigarette consumption. In a specific histological cell type analysis, a positive association was found for each subtype of lung cancer, with no appreciable difference between cell types. In summary, our study demonstrated that the MspI variant CYP1A1 genotype is significantly associated with an increased risk of lung cancer among Caucasians with the odds ratio approximately, equivalent to 2 after controlling for important confounding factors. These results are similar to those obtained from reanalysis of published data on the combined CYP1A1 genotypes in a Japanese population (combined odds ratio, 1.95; 95% confidence interval, 1.17-3.28). Moreover, the elevated risk is noted in heterozygotes, i.e., individuals who carry only one copy of the variant gene.

Aged↗
PubMed1995

Correlation of DNA adducts in blood mononuclear cells with tobacco carcinogen-induced damage in human lung.

The formation of carcinogen-DNA adducts within the respiratory epithelium is thought to be a critical factor in the induction of lung cancer from tobacco smoke. A reliable surrogate measure of carcinogen damage to the lung would be of great value in molecular epidemiological studies of cancer risk. The validity of measurements of DNA adducts formed from hydrophobic aromatic hydrocarbons in peripheral blood mononuclear cells (MNCs) was investigated by comparing the levels of aromatic DNA adducts detected in lung tissue from 31 lung cancer patients with those detected in MNCs from the same individuals using the 32P-postlabeling assay. The associations of smoking history and intake of dietary antioxidants with adduct levels also were assessed. Tissue-specific, as well as common DNA adducts were detected in lung and blood; total MNC adduct levels were highly correlated with total lung adducts. After smoking cessation, adduct levels appeared to decay in both tissues at similar rates. Multivariate analyses (Poisson regression modeling) indicated that dietary antioxidant intake (carotenoids, vitamin A, and retinol) modified the levels of aromatic DNA adducts in both the lungs and blood. Of all models tested, the optimal one for predicting lung adduct levels included the measure of blood MNC adduct levels only. Therefore, blood MNCs are a valid surrogate tissue for estimating the burden of DNA adducts in respiratory tissue in molecular epidemiological studies.

Aged↗
PubMed1995

Asbestos-related diseases in construction carpenters.

To assess the association of minimal parenchymal fibrosis and pleural plaques with respiratory functional impairment, we conducted a survey of 631 asbestos-exposed construction carpenters. This population had a relatively low prevalence of radiographic abnormalities and lung function impairment. Pleural plaques was the asbestos-related disease most prevalent, followed by interstitial fibrosis with predominantly low profusion scores. The most frequent functional impairment was the obstructive pattern, followed by restrictive and mixed patterns. After adjusting for potential confounders, the presence of pleural plaques was significantly associated with a mixed respiratory pattern of impairment (OR = 3.7, 95% CI 1.4-12.3). Furthermore, our data were consistent with a weak association between pleural plaques and a predominantly restrictive defect (OR-1.3, 95% CI 0.4-3.9). This study also suggested an association between minimally detectable profusions and both obstructive (OR = 1.9, 95% CI 0.6-6.3) and mixed (OR = 1.6, 95% CI 0.3-7.1) defects. Although only 631 of a potential 7,649 active and retired union members participated in this first-time survey and were relatively young, these findings add new evidence to the functional importance of pleural fibrosis and minimal parenchymal fibrosis.

Adult↗
PubMed1995

Mutant frequency at the hprt locus in human lymphocytes in a case-control study of lung cancer.

A clonal assay to determine the mutant frequency (MF) at the hypoxanthine-guanine phosphoribosyl transferase (hprt) locus in human lymphocytes has been used by a number of investigators to study exposure to mutagens and carcinogens in a variety of populations. We have studied hprt MF in 106 subjects (40 controls and 66 cases) enrolled in a case-control investigation of lung cancer. Epidemiological data collected included smoking history, intake of dietary micronutrients, and occupational and environmental exposures as well as medical history, all obtained from an interviewer-administered questionnaire. All subjects were also genotyped for the known polymorphism in glutathione S-transferase class mu (GST-mu). In analysis of cases and controls, hprt MF was not associated with age, smoking, the polymorphism in GST mu, dietary intake, occupational exposures, family history of cancer or usage of medications. Since MF and cloning efficiency (CE) are not independent when CE is low, further analysis in cases and controls with a CE greater than or equal to 30% (27 cases and 22 controls) was also conducted. In analysis of controls, hprt MF increased with age and was inversely associated with intake of folate and vitamins A and C. The presence of lung cancer was not associated with hprt MF. Thus, our study supports the previous observation that dietary components may affect the MF at the hprt locus.

Age Factors↗
PubMed1995

Comparison of sister chromatid exchange frequency in peripheral lymphocytes in lung cancer cases and controls.

Cytogenetic alterations have been associated with the occurrence of many cancers. However, limited data exist to address whether increased chromosomal changes in surrogate normal tissue are similarly associated with malignancy. As part of an ongoing case-control study of lung cancer, we have studied the factors that affect sister chromatid exchange (SCE) frequency in lymphocytes from lung cancer patients. Further, we sought to investigate whether the factors that affect SCE frequencies were comparable in lung cancer cases and controls. Cases had newly diagnosed, operable primary lung cancer. Controls were friends and spouses of cases. Detailed information on smoking, family history of cancer, medical history, and environmental and occupational exposures was obtained in an interviewer-administered questionnaire. Intake of antioxidants was also determined through the administration of a validated semiquantitative food frequency questionnaire. Metabolic traits studied included the polymorphic glutathione-S-transferase class mu (GST-mu) and variants of P450 isoenzymes CYP1A1 and CYP 2D6. Overall, 78 cases and 78 controls were included in the analysis. Although there was a small number of lung cancer patients who had never smoked in the study (9% of cases), these patients had higher SCE frequencies than current or former smokers. This suggests that factors associated with genomic instability may also play a role in the pathogenesis of lung cancer. The best fit model for SCE frequency, which had been previously generated from control data alone, included age, gender, smoking, GST-mu, and vitamin A intake. However, when this model was applied to lung cancer patients, smoking was not associated with an elevated SCE frequency. Thus, it is not clear that SCE frequency data in prevalent lung cancer cases and controls are comparable.

Age Factors↗
PubMed1995

Ethnic differences in the prevalence of the homozygous deleted genotype of glutathione S-transferase theta.

In humans the glutathione S-transferase (GST) genes encode four classes of proteins (GST) important in the detoxification of reactive electrophiles. Recently, a gene deletion polymorphism was discovered within the GST class theta locus that leads to a functional deficiency in GST theta activity within circulating red blood cells. In this study we have examined the ethnic distribution of this polymorphism using a polymerase chain reaction (PCR)-based genotyping method. Five different ethnic groups were studied: North American Caucasians, African-Americans, Mexican-Americans, Chinese and Koreans. The prevalence of the null genotype was highest among Chinese (64.4%), followed by Koreans (60.2%), African-Americans (21.8%) and Caucasians (20.4%), whereas the prevalence was lowest among Mexican-Americans (9.7%). Interestingly, the prevalence of the deleted genotype in Caucasians differed significantly when 257 individuals drawn from a nation wide organization were compared with 185 people from the New England area (23.7 versus 15.7%, P < 0.05, chi 2 test). These results indicate that there are major differences in the prevalence of this trait attributable to ethnicity and that ethnic origin even among Caucasians should be considered in studies of gene-environment interaction involving this polymorphism.

Asian People↗
PubMed1995

Upper airway response in workers exposed to fuel oil ash: nasal lavage analysis.

OBJECTIVES: Among other constituents, fuel oil ash contains vanadium pentoxide, a known respiratory irritant. Exposure to ambient vanadium pentoxide dust has been shown to produce irritation of the eyes, nose, and throat. The usefulness of nasal lavage in detecting an inflammatory response to exposure to fuel oil ash among 37 boilermakers and utility workers was investigated. METHODS: A baseline lavage was performed on the morning of the first day back to work after an average of 114 days away from work (range 36 hours to 1737 days). A lavage was performed after exposure on the morning three days after the baseline lavage. Exposure to respirable particulate matter of diameter < or = 10 microns (PM10) and respirable vanadium dust were estimated with daily work diaries and a personal sampling device for respirable particulates. These estimates were made for each subject on each workday during the three days between lavages. For each subject, the adjusted change in polymorphonuclear cells was calculated by dividing the change in polymorphonuclear cell counts by the average of the counts before and after exposure. The association between the adjusted polymorphonuclear cell counts and exposure was assessed with multiple linear regression, adjusted for age and current smoking. RESULTS: Personal sampling (one to 10 hour time weighted average) showed a range of PM10 concentrations of 50 to 4510 micrograms/m3, and respirable vanadium dust concentration of 0.10 to 139 micrograms/m3. In smokers the adjusted polymorphonuclear cell count was not significantly different from zero (-0.1%, P > 0.5), but in nonsmokers it was significantly greater than zero (+50%, P < 0.05). In both non-smokers and smokers, there was considerable variability in adjusted polymorphonuclear cell counts and a dose-response relation between these adjusted cell counts and either PM10 or respirable vanadium dust exposure could not be found. CONCLUSION: A significant increase in polymorphonuclear cells in non-smokers but not smokers was found. This suggests that in non-smokers, exposure to fuel oil ash is associated with upper airway inflammation manifested as increased polymorphonuclear cell counts. The lack of an increase in polymorphonuclear cells in smokers may reflect either a diminished inflammatory response or may indicate that smoking masks the effect of exposure to fuel oil ash.

Adult↗
PubMed1995

Airway obstruction in boilermakers exposed to fuel oil ash. A prospective investigation.

We prospectively investigated the lower airway response in boilermakers overhauling an oil-powered boiler. We studied 26 male boilermakers with a mean age (SD) of 43.3 (8.6) yr. Pre-exposure spirometry and methacholine challenge tests were performed before beginning the boiler overhaul; postexposure tests were performed after approximately 4 wk of work on the boiler. Exposure to particulates with an aerodynamic diameter of 10 microns and smaller (PM10) and respirable vanadium dust were estimated using daily work diaries and a personal sampling device for respirable particles. Using these estimates, we calculated average and peak exposure between pre- and postexposure tests for each subject. The average PM10 concentration ranged from 1.44 to 6.69 mg/m3, with a mean (SD) of 3.22 (1.42) mg/m3; the average vanadium concentration ranged from 2.2 to 31.3, with a mean (SD) of 12.2 (9.1) micrograms/m3. The mean postexposure fall in FEV1 was 140 +/- 160 ml (p < 0.01); 24 of 26 subjects had a drop in FEV1. For each subject, the adjusted change in FEV1 (delta FEV1.adj) was calculated by dividing the change in FEV1 by the average of the pre- and postexposure FEV1 values. The delta FEV1.adj was regressed, controlling age and current smoking status, on average and peak exposure to both PM10 and vanadium. There was a dose-response relationship between average and peak PM10 exposure and delta FEV1.adj: beta = -0.91% per mg/m3, p = 0.08 and beta = -1.03% per mg/m3, p = 0.03, respectively. However, there was no relationship between delta FEV1.adj and respirable vanadium dust concentration. Furthermore, there was no postexposure change in nonspecific airway responsiveness. In summary, we found a significant fall in FEV1 and a dose-response relationship between delta FEV1.adj and average and peak PM10 exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Are reference intervals for carboxyhemoglobin appropriate? A survey of Boston area laboratories.

CO is a leading cause of poisoning deaths in the US today. Treating physicians use the carboxyhemoglobin (COHb) % saturation to guide the diagnosis and treatment of CO intoxication. We conducted a telephone survey of hospitals and laboratories in the Boston area, focusing on methodology for COHb determination and accompanying COHb reference intervals. Among 130 facilities, 23 (18%) provide COHb analysis. All facilities that perform the COHb test utilize dedicated multiwave-length photometry. Reference intervals for COHb varied widely among facilities. Eight of 21 (38%) facilities give unacceptably high "normal intervals" for nonsmokers when compared with values available in the literature. Thirteen of 20 (65%) use reference intervals for smokers that are too low, and 3 of 20 (15%) use values that are too high. These reference values provided by the testing facilities may be misleading to the ordering physicians unfamiliar with background COHb saturations. This may lead to misdiagnoses, false reassurances, and perhaps less aggressive treatment than might be warranted. The results of this study argue for wider adoption of COHb reference intervals supported by the current literature.

Boston↗
PubMed1994

Use of state workers' compensation data for occupational carpal tunnel syndrome surveillance: a feasibility study in Massachusetts.

The purpose of this study was to determine the feasibility of using Massachusetts workers' compensation data for passive surveillance of occupational carpal tunnel syndrome (OCTS). Workers' compensation claims for OCTS (n = 358) and for possible cases of OCTS (n = 1,121) active during the first 6 months of 1989 were identified. The availability and distribution of demographic and employment descriptors were assessed. Medical records on a sample of the claims were reviewed to validate the diagnosis of OCTS. Age, gender, and occupation were available for less than 47% of the reported cases of OCTS. The majority (88%) of cases on whom medical record review was performed had a physician's diagnosis of carpal tunnel syndrome (CTS), and most of this group had confirmatory nerve conduction studies or electromyography. However, there were fundamental limitations to workers' compensation based disease surveillance in Massachusetts, including underascertainment of cases, potential ascertainment biases, delayed case reporting, limited access to specific diagnostic information, and incomplete and sometimes inaccurate information. These limitations are likely to be applicable in many, if not most, states and must be made clear in any analyses based on workers' compensation data.

Adolescent↗
PubMed1994

Genotoxicity to human cells induced by air particulates isolated during the Kuwait oil fires.

In an effort to examine the potential of exposure to soot from the 1991 oil fires in the Kuwait desert for inducing genetic effects we studied the in vitro genotoxicity of this material. Air particulates isolated near the Kuwait oil fires were studied using three assays. Dose-dependent increases were observed for both sister chromatid exchanges in human peripheral blood lymphocytes and mutation at the hprt locus in the metabolically competent human lymphoblast cell line AHH-1. Similar magnitudes of response were seen using these two assays when testing a standard air particulate sample which had been isolated from the Washington, DC, area. Using the 32P-postlabeling assay, no increase in DNA adduct formation was observed in AHH-1 cells treated with particulates isolated from sampling in Kuwait.

Air Pollutants↗
PubMed1994

Respiratory disease in cotton textile workers: epidemiologic assessment of small airway function.

We performed a cross-sectional study of 705 textile workers in two cotton mills and one silk mill in Shanghai, People's Republic of China, to assess small airway function among cotton textile workers and to compare the FEV1 to the FEF25-75 in detecting airflow obstruction in these workers. All workers had at least 2 years of work experience. Environmental sampling was performed with vertical elutriators and revealed that in the cotton mills mean elutriated dust levels were 1.07 +/- 0.23 mg/m3 in mill 1 and 1.01 mg/m3 +/- 0.24 mg/m3 in mill 2. Mean endotoxin levels were 332 +/- 83 ng/m3 in mill 1 and 101 +/- 46 ng/m3 in mill 2. No differences were found in preshift FEV1 or FEF25-75 between cotton and silk workers. Cotton workers had significantly greater declines than silk workers in FEV1 across a workshift, but not in FEF25-75. These acute changes in FEV1 were noted in both byssinotic and nonbyssinotic workers. Although cotton dust may affect both large and small airways, spirometric measures of small airway function (e.g., FEF25-75) add little to the FEV1 and FVC in detecting airflow limitation in cotton dust-exposed workers.

Adult↗