Relationships between inhalable and total hexavalent chromium exposures in steel passivation, welding and electroplating operations of Ontario.

The main aim of the study was to assess the relationship between inhalable hexavalent chromium and "total" hexavalent chromium. Air sampling was conducted at steel passivation operation of a steel manufacturer at a stainless steel welding operation and at two hard chrome electroplaters. Air samples were taken side-by-side for "total" dust using closed-face 37-mm diameter cassette samplers and for inhalable dust using Institute of Occupational Medicine inhalable samplers. A total of 40 pairs of total and inhalable dust samples were collected and later analyzed. The range of "total" dust and inhalable dust concentrations in µg/m3 measured were 30-410 and 0.02 to 740 respectively for steel passivation; 260 to 1520 and 477 to 6970 for welding; and 0.01 to 1500 and 204 to 2130 for electroplaters. The range of "total" dust hexavalent chromium and inhalable dust hexavalent chromium concentrations in µg/m3 were 0.02-89 and 0.02 to 150 respectively for steel making; 4.1 to 4.9 and 2.2 to 6.9 for welding and 0.01 to 9.3 and 0.01 to 21 for electroplaters. A linear relationship between inhalable hexavalent chromium and "total" hexavalent chromium was found with a slope of 1.4 (CI:1.3, 1.5) and 0 offset. A ratio of 1.4 can thus be used as a conversion factor to convert previous data of hexavalent chromium taken on "total" dust basis to inhalable hexavalent chromium concentrations.

Aluminum in the lungs of Ontario hardrock miners.

The objective of this study was to determine the concentration of aluminum in the autopsied lungs of eight hardrock miners. These miners had inhaled McIntyre Powder (a mixture of aluminum and aluminum oxide) as a prophylaxis against silicosis. The study involved chemical analysis of lungs, where each whole lung was divided horizontally into three sections and analyzed by atomic absorption spectrophotometer equipped with a graphite furnace. The grand mean level of aluminum was found to be 476.4 µg/g of dry tissue, which is similar in the range reported for occupationally exposed groups. The effect of smoking was also examined and found to be unrelated. This study provides an estimate of retained aluminum in the lungs of Ontario hardrock miners as a result of occupational exposure to hardrock mining environment and inhalation of McIntyre Powder.

Feasibility and Safety of Multicenter Tissue and Biofluid Sampling for α-Synuclein in Parkinson's Disease: The Systemic Synuclein Sampling Study (S4).

BACKGROUND: α-synuclein is a lead Parkinson's disease (PD) biomarker. There are conflicting reports regarding accuracy of α-synuclein in different tissues and biofluids as a PD biomarker, and the within-subject anatomical distribution of α-synuclein is not well described. The Systemic Synuclein Sampling Study (S4) aims to address these gaps in knowledge. The S4 is a multicenter, cross-sectional, observational study evaluating α-synuclein in multiple tissues and biofluids in PD and healthy controls (HC). OBJECTIVE: To describe the baseline characteristics of the S4 cohort and safety and feasibility of this study. METHODS: Participants underwent motor and non-motor clinical assessments, dopamine transporter SPECT, biofluid collection (cerebrospinal fluid, saliva, and blood), and tissue biopsies (skin, sigmoid colon, and submandibular gland). Biopsy adequacy was determined based on presence of adequate target tissue. Tissue sections were stained with the 5C12 monoclonal antibody against unmodified α-synuclein. All specimens were acquired and processed in a standardized manner. Adverse events were systematically recorded. RESULTS: The final cohort consists of 82 participants (61 PD, 21 HC). In 68 subjects (83%), all types of specimens were obtained but only 50 (61%) of subjects had all specimens both collected and evaluable for α-synuclein. Mild adverse events were common, especially for submandibular gland biopsy, but only 1 severe adverse event occurred. CONCLUSION: Multicenter tissue and biofluid sampling for α-synuclein is feasible and generally safe. S4 will inform understanding of the concurrent distribution of α-synuclein pathology and biomarkers in biofluids and peripheral nervous system in PD.

Evaluation of Firefighter Exposure to Wood Smoke during Training Exercises at Burn Houses.

Smoke from wood-fueled fires is one of the most common hazards encountered by firefighters worldwide. Wood smoke is complex in nature and contains numerous compounds, including methoxyphenols (MPs) and polycyclic aromatic hydrocarbons (PAHs), some of which are carcinogenic. Chronic exposure to wood smoke can lead to adverse health outcomes, including respiratory infections, impaired lung function, cardiac infarctions, and cancers. At training exercises held in burn houses at four fire departments across Ontario, air samples, skin wipes, and urine specimens from a cohort of firefighters (n = 28) were collected prior to and after exposure. Wood was the primary fuel used in these training exercises. Air samples showed that MP concentrations were on average 5-fold greater than those of PAHs. Skin wipe samples acquired from multiple body sites of firefighters indicated whole-body smoke exposure. A suite of MPs (methyl-, ethyl-, and propylsyringol) and deconjugated PAH metabolites (hydroxynaphthalene, hydroxyfluorene, hydroxyphenanthrene, and their isomers) were found to be sensitive markers of smoke exposure in urine. Creatinine-normalized levels of these markers were significantly elevated (p < 0.05) in 24 h postexposure urine despite large between-subject variations that were dependent on the specific operational roles of firefighters while using personal protective equipment. This work offers deeper insight into potential health risk from smoke exposure that is needed for translation of better mitigation policies, including improved equipment to reduce direct skin absorption and standardized hygiene practices implemented at different regional fire services.

Retrospective Exposure Assessment for Occupational Disease of an Individual Worker Using an Exposure Database and Trend Analysis.

This article outlines a hierarchy of data required for retrospective exposure assessment for occupational disease of an individual worker. It then outlines in a step-wise manner how trend analysis using a relatively large exposure database can be used to estimate such exposure. The process of how a large database containing exposure measurements can be prepared for estimating historic occupational exposures of individual workers in relation to their illnesses is described. The asbestos subset from a large government collected air monitoring database called Medical Surveillance (MESU) was selected to illustrate the cleaning and analysis processes. After unidentifiable values were removed, the cleaned dataset was examined for possible sources of variability such as changes to sampling protocol. Limit of detection (LOD) values were substituted for all non-detectable values prior to the calculation of descriptive statistic using left censored analysis methods (i.e., maximum likelihood estimation (MLE), Kaplan Meier (KM), and simple substitution). The JoinPoint Regression Program was used to perform trend analysis and calculate an annual percentage change (APC) value for the available sampling period. An asbestos case study is presented to illustrate how the APC can then be combined with more recent job and/or process specific exposure data to estimate historic levels. The MESU asbestos dataset contained 1,610 samples from 1984-1995. An average of 17% of this data was left censored. The asbestos air sampling methods in Ontario changed around 1990. LOD values of 0.06 f/cc and 0.02 f/cc were substituted for LOD values pre- and post-1990, respectively. The annual mean fiber levels for the MLE method were an average of 44% lower than KM and substitution methods. The corresponding APC for MLE method was -6.5% and -7.7% for KM and simple substitution. The findings of this paper illustrate how the temporal trend of an exposure databases can be used to efficiently estimate historic contaminant levels in the presence of limited historical information.

Metals in the lungs of Ontario hardrock miners.

The objective of this study was to determine the concentration of nickel, cadmium, and lead in the autopsied lungs of 29 hardrock miners. It involved chemical analysis of the lungs, where each lung was divided horizontally into 3 sections and analyzed by an atomic absorption spectrophotometer equipped with a graphite furnace. The grand mean levels of nickel, cadmium, and lead were found to be 1.84, 1.74, and 2.75 µg/g of dry tissue, respectively. The effect of smoking was also examined. The ratios using the mean values between smoker and nonsmoker for nickel, cadmium, and lead were found to be 0.7, 5.4, and 1.4, respectively. The level of cadmium in smokers was significantly higher than nonsmokers. This study provides an estimate of retained metals in the lungs of the Ontario hardrock miners as a result of occupational exposure to hardrock mining environment.

The first 5-year follow up of distal antegrade continence enema stomas.

AIM: We investigated 5-year results of distal sites for antegrade continence enemas (DACE). METHODS: Patients with DACE sites placed more than 5 years previously were identified. Details of procedures were obtained. Parents, and patients over 18, were telephoned and asked to answer a standardised questionnaire. RESULTS: 31 patients were identified. Median age at DACE placement was 7 years (range 3-20). Median follow up was 92 months (range 66-145). 22 tubes were placed endoscopically, 7 were placed at open surgery and 2 at laparoscopic surgery. 28 responses to the telephone questionnaire were obtained. Of these, 15 were still using their DACE and 13 had stopped. Of those who had ceased washouts: 7 reported resolution of symptoms, 4 had a colostomy, 1 an ileostomy and 1 patient had abandoned their DACE. In patients using their stoma, washouts took a median of 5 min, with a median time to result of 25 min. 10 patients reported no soiling, 4 monthly and 1 daily soiling. Median satisfaction score was 8/10 (range 1-10/10). 24 (85%) said that they would recommend a DACE. CONCLUSIONS: This is the first report of 5-year follow up of a series of patients performing DACE washouts. The results are encouraging.

Nicotine and estrogen synergistically exacerbate cerebral ischemic injury.

The greater incidence of myocardial infarction, cardiac arrest, and ischemic stroke among women who smoke and use oral contraception (OC) compared to women who do not smoke and who do or do not use OC may be due in part to how nicotine influences endocrine function in women. For example, we recently demonstrated that chronic exposure to nicotine, the addictive agent in tobacco smoke responsible for the elevated risk of cardiac arrest, abolishes the endogenous or exogenous 17ß-estradiol-conferred protection of the hippocampus against global cerebral ischemia (a potential outcome of cardiac arrest) in naive or ovariectomized female rats. In the current study we examined the hypotheses that (1) a synergistic deleterious effect of nicotine plus oral contraceptives exacerbates post-ischemic hippocampal damage in female rats, and (2) nicotine directly inhibits estrogen-mediated intracellular signaling in the hippocampus. To test first hypothesis and to simulate smoking behavior-induced nicotine levels in the human body, we implanted osmotic pumps containing nicotine in the female rats for 16 days. Furthermore, we mimicked the use of oral contraceptives in females by administering oral contraceptives orally to the rat. Rats exposed to either nicotine alone or in combination with oral contraceptives were subjected to an episode of cerebral ischemia and the resultant brain damage was quantified. These results showed for the first time that nicotine with oral contraceptives did indeed exacerbate post-ischemic CA1 damage as compared to nicotine alone in naive female rats. In ex vivo hippocampal slice cultures, we found that nicotine alone or with 17ß-estradiol directly hinders estrogen receptors-mediated phosphorylation of cyclic-AMP element binding protein, a process required for neuronal survival and also exacerbates ischemic damage. Thus, nicotine can affect the outcome of cerebral ischemia by influencing brain endocrine function directly rather than through indirect systemic effects.

Silica exposure assessment in a mortality study of Vermont granite workers.

A study of past silica and respirable dust exposures in the Vermont granite industry was conducted to develop a job exposure matrix (JEM) that used 5204 industrial hygiene measurements made from 1924-2004. The construction of the JEM involved data entry from several original sources into an Excel database that was reviewed later to ensure accuracy. Exposure measurements by job or location were grouped in two broad categories of quarry or shed and then into 22 job classes. Missing exposure data by time period were computed, taking into account improvements in dust control and periods of significant reduction in dustiness. Percent free silica (α-quartz) in respirable dust was estimated to be 11.0% based on previous published studies in Vermont and on data in the current database. About 60% of all measurement data (primarily from years prior to 1972) were obtained using the impinger and expressed in millions of particles per cubic foot (mppcf), which were converted to equivalent respirable free silica concentrations using the conversion of 10 mppcf = 0.1 mg/m(3) of respirable silica. For impinger data, respirable dust was calculated by multiplying respirable silica by a factor of 9.091 to reflect that the respirable silica was 11.0% respirable dust. This JEM has been used in a recent epidemiologic study to assess mortality in Vermont granite workers and to examine the relationships among mortality from silicosis, lung cancer, and other nonmalignant respiratory diseases.

Mortality in Vermont granite workers and its association with silica exposure.

OBJECTIVES: To assess mortality in Vermont granite workers and examine relationships between silica exposure and mortality from lung cancer, kidney cancer, non-malignant kidney disease, silicosis and other non-malignant respiratory disease. Methods Workers employed between 1947 and 1998 were identified. Exposures were estimated using a job-exposure matrix. Mortality was assessed through 2004 and standardised mortality ratios (SMRs) were computed. Associations between mortality and exposure to silica were assessed by nested case-control analyses using conditional logistic regression. Results 7052 workers had sufficient data for statistical analysis. SMRs were significantly elevated for lung cancer (SMR 1.37, 95% CI 1.23 to 1.52), silicosis (SMR 59.13, 95% CI 44.55 to 76.97), tuberculosis (SMR 21.74, 95% CI 18.37 to 25.56) and other non-malignant respiratory disease (SMR 1.74, 95% CI 1.50 to 2.02) but not for kidney cancer or non-malignant kidney disease. In nested case-control analyses, significant associations with cumulative exposure to respirable free silica were observed for silicosis (OR 1.13, 95% CI 1.05 to 1.21 for each 1 mg/m(3)-year increase in cumulative exposure) and other non-malignant respiratory disease (OR 1.10, 95% CI 1.03 to 1.16) but not for lung cancer (OR 0.99, 95% CI 0.94 to 1.03), kidney cancer (OR 0.96, 95% CI 0.84 to 1.09) or non-malignant kidney disease (OR 0.95, 95% CI 0.84 to 1.08). Conclusions Exposure to crystalline silica in Vermont granite workers was associated with increased mortality from silicosis and other non-malignant respiratory disease, but there was no evidence that increased lung cancer mortality in the cohort was due to exposure. Mortality from malignant and non-malignant kidney disease was not significantly increased or associated with exposure.

Resveratrol pretreatment protects rat brain from cerebral ischemic damage via a sirtuin 1-uncoupling protein 2 pathway.

Resveratrol is a natural polyphenol found in grapes and wine and has been associated with protective effects against cardiovascular diseases. In vitro, both resveratrol preconditioning (RPC) and ischemic preconditioning (IPC) require activation of sirtuin 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase, to induce neuroprotection against cerebral ischemia. In the present study, we tested two hypotheses: (a) that neuroprotection against cerebral ischemia can be induced by RPC in vivo; and (b) that RPC neuroprotection involves alterations in mitochondrial function via the SIRT1 target mitochondrial uncoupling protein 2 (UCP2). IPC was induced by 2 min of global ischemia (temporary bilateral carotid artery occlusion with hypotension), and RPC, by i.p. injection of resveratrol at 10, 50 and 100 mg/kg dosages. Forty-eight hours later, we compared the neuroprotective efficacy of RPC and IPC in vulnerable cornu ammonis 1 hippocampal pyramidal neurons using a rat model of asphyxial cardiac arrest (ACA). SIRT1 activity was measured using a SIRT1-specific fluorescent enzyme activity assay. In hippocampal mitochondria isolated 48 h after IPC or RPC, we measured UCP2 levels, membrane potential, respiration, and the mitochondrial ATP synthesis efficiency (ADP/O ratio). Both IPC and RPC induced tolerance against brain injury induced by cardiac arrest in this in vivo model. IPC increased SIRT1 activity at 48 h, while RPC increased SIRT1 activity at 1 h but not 48 h after treatment in hippocampus. Resveratrol significantly decreased UCP2 levels by 35% compared to sham-treated rats. The SIRT1-specific inhibitor sirtinol abolished the neuroprotection afforded by RPC and the decrease in UCP2 levels. Finally, RPC significantly increased the ADP/O ratio in hippocampal mitochondria reflecting enhanced ATP synthesis efficiency. In conclusion, in vivo resveratrol pretreatment confers neuroprotection similar to IPC via the SIRT1-UCP2 pathway.

Pretreatment with a single estradiol-17beta bolus activates cyclic-AMP response element binding protein and protects CA1 neurons against global cerebral ischemia.

Estradiol-17beta is released from the ovaries in a cyclic manner during the normal estrous cycle in rats. During the transition from the diestrous to proestrous stage, the 17beta-estradiol increases in blood circulation. We hypothesized that a higher serum level of endogenous 17beta-estradiol would protect hippocampal pyramidal neurons against global cerebral ischemia via activation of the cyclic-AMP response element binding protein (CREB)-mediated signaling cascade. Furthermore, we asked if a single 17beta-estradiol bolus provides protection against ischemia in the absence of endogenous estradiol. To test these hypotheses, rats were subjected to global cerebral ischemia at different stages of the estrous cycle. Ischemia was produced by bilateral carotid occlusion and systemic hypotension. Brains were examined for histopathology at 7 days of reperfusion. Higher serum levels of 17beta-estradiol (at proestrus and estrus stages) correlated with increased immunoreactivity of pCREB in hippocampus and ischemic tolerance. At diestrus, when circulating gonadal hormone concentrations were lowest, the pCREB protein content of hippocampus was reduced and showed the least number of normal neurons after ischemia compared to other stages of the estrous cycle. A similar phosphorylation pattern was also observed for mitogen-activated protein kinase (MAPK) and calcium-calmodulin-dependent protein kinase (CaMKII) in hippocampus. The cyclic variation in ovarian hormones did not reflect phosphorylation of protein kinase B (Akt). To test the efficacy of a single bolus of 17beta-estradiol before ischemia, ovariectomized rats were treated with 17beta-estradiol (5/10/50 microg/kg) or vehicle (oil) and 48/72/96 h later rats were exposed to cerebral ischemia. A single 17beta-estradiol bolus treatment in ovariectomized rats significantly increased CREB mRNA activation and protected CA1 pyramidal neurons against ischemia. These results suggest that an exogenous bolus of 17beta-estradiol to ovariectomized rats protects hippocampus against ischemia via activation of the CREB pathway in a manner similar to the endogenous estrous cycle.

Dust content of lungs and its relationships to pathology, radiology and occupational exposure in Ontario hardrock miners.

BACKGROUND: Autopsied lungs from 29 hard rock miners were investigated to determine the relationship of the dust content to pathology, radiology, and occupational exposure. METHODS: Each lung was divided horizontally into three sections. Pathological and radiological studies and chemical analyses were carried out on samples from each section. The hilar lymph nodes were also studied chemically. The work history and smoking history were assessed. The occupational exposure to silica and total dust were estimated. The effect of smoking was examined, and the relationship between dust content of the lungs to that of the lymph nodes were also investigated. RESULTS: There was a good agreement between radiologic and pathologic findings. Positive correlations were seen between hydroxyproline (as an index of fibrosis), silica dust, non-silica inorganic dust, radiographic category of pneumoconiosis and pathologic grade of silicosis. Smokers lost on average 7 years of life compared to non-smokers, but numbers were small and no adjustment was made. Silica appeared to be concentrated in lungs and lymph nodes compared to the estimates of silica concentration in the mining environment. Silica in the lymph nodes on average is 2.4-fold higher than in the lungs. CONCLUSIONS: This study of autopsied hard rock miners lungs shows positive relationships between lung dust and hydroxyproline content, radiological and pathological findings.

Evolution of sensory structures in basal metazoa.

Cnidaria have traditionally been viewed as the most basal animals with complex, organ-like multicellular structures dedicated to sensory perception. However, sponges also have a surprising range of the genes required for sensory and neural functions in Bilateria. Here, we: (1) discuss "sense organ" regulatory genes, including; sine oculis, Brain 3, and eyes absent, that are expressed in cnidarian sense organs; (2) assess the sensory features of the planula, polyp, and medusa life-history stages of Cnidaria; and (3) discuss physiological and molecular data that suggest sensory and "neural" processes in sponges. We then develop arguments explaining the shared aspects of developmental regulation across sense organs and between sense organs and other structures. We focus on explanations involving divergent evolution from a common ancestral condition. In Bilateria, distinct sense-organ types share components of developmental-gene regulation. These regulators are also present in basal metazoans, suggesting evolution of multiple bilaterian organs from fewer antecedent sensory structures in a metazoan ancestor. More broadly, we hypothesize that developmental genetic similarities between sense organs and appendages may reflect descent from closely associated structures, or a composite organ, in the common ancestor of Cnidaria and Bilateria, and we argue that such similarities between bilaterian sense organs and kidneys may derive from a multifunctional aggregations of choanocyte-like cells in a metazoan ancestor. We hope these speculative arguments presented here will stimulate further discussion of these and related questions.

Apple polygalacturonase inhibiting protein1 expressed in transgenic tobacco inhibits polygalacturonases from fungal pathogens of apple and the anthracnose pathogen of lupins.

Extracts from apple fruit (cultivar "Granny Smith") inhibited the cell-wall degrading polygalacturonase (PG) activity of Colletotrichum lupini, the causal agent of anthracnose on lupins, as well as Aspergillus niger PG. Southern blot analysis indicated that this cultivar of apple has a small gene family of polygalacturonase inhibiting proteins (pgips), and therefore heterologous expression in transgenic tobacco was used to identify the specific gene product responsible for the inhibitory activity. A previously isolated pgip gene, termed Mdpgip1, was introduced into tobacco (Nicotiana tabacum) by Agrobacterium-mediated transformation. The mature MdPGIP1 protein was purified to apparent homogeneity from tobacco leaves by high salt extraction, clarification by DEAE-Sepharose and cation exchange HPLC. Purified MdPGIP1 inhibited PGs from C. lupini and PGs from two economically important pathogens of apple trees, Botryosphaeria obtusa and Diaporthe ambigua. It did not inhibit the A. niger PG, which was in contrast to the apple fruit extract used in this study. We conclude that there are at least two active PGIPs expressed in apple, which differ in their charge properties and ability to inhibit A. niger PG.

An evaluation of analytical methods, air sampling techniques, and airborne occupational exposure of metalworking fluids.

This article summarizes an assessment of air sampling and analytical methods for both oil and water-based metalworking fluids (MWFs). Three hundred and seventy-four long-term area and personal airborne samples were collected at four plants using total (closed-face) aerosol samplers and thoracic samplers. A direct-reading device (DustTrak) was also used. The processes sampled include steel tube making, automotive component manufacturing, and small part manufacturing in a machine shop. The American Society for Testing and Materials (ASTM) Method PS42-97 of analysis was evaluated in the laboratory. This evaluation included sample recovery, determination of detection limits, and stability of samples during storage. Results of the laboratory validation showed (a) the sample recovery to be about 87%, (b) the detection limit to be 35 microg, and (c) sample stability during storage at room temperature to decline rapidly within a few days. To minimize sample loss, the samples should be stored in a freezer and analyzed within a week. The ASTM method should be the preferred method for assessing metalworking fluids (MWFs). The ratio of thoracic aerosol to total aerosol ranged from 0.6 to 0.7. A similar relationship was found between the thoracic extractable aerosol and total extractable aerosol. The DustTrak, with 10-microm sampling head, was useful in pinpointing the areas of potential exposure. MWF exposure at the four plants ranged from 0.04 to 3.84 mg/m3 with the geometric mean ranging between 0.22 to 0.59 mg/m3. Based on this data and the assumption of log normality, MWF exposures are expected to exceed the National Institute for Occupational Safety and Health recommended exposure limit of 0.5 mg/m3 as total mass and 0.4 mg/m3 as thoracic mass about 38% of the time. In addition to controlling airborne MWF exposure, full protection of workers would require the institution of programs for fluid management and dermal exposure prevention.

Occupational exposure limits: an approach and calculation aid for extended work schedule adjustments.

Past reviews of occupational exposure limit (OEL) adjustments have covered both decision logic and calculation methods to derive factors to assure protection of workers on extended (also known as unusual) work shifts. The approaches reviewed included several Haber's rule based methods, several variants of single compartment toxicokinetic (TK) models, and physiologically based pharmacokinetic modeling. These models calculate OEL adjustment factors based on the work shift and the uptake and elimination of the toxicant. A key parameter of the TK models is the biologic half-life of the toxicant, but reliable data for the half-life are not available for all substances of concern. A spreadsheet is presented that implements TK calculations, with one of the presented TK calculation alternatives not dependent on half-life data. This half-life data independent approach is suggested as a viable option for situations when the toxicant's half-life is unknown or uncertain.

Mortality among Ontario members of the International Union of Bricklayers and Allied Craftworkers.

BACKGROUND: Dust exposed workers may be at increased risk of pneumoconiosis, stomach cancer, lung cancer, and obstructive lung disease. Bricklayers may experience high exposures to silica and inorganic dusts. The aim of this study was to examine the mortality pattern of bricklayers to identify occupational associations with mortality. METHODS: A cohort of 10,953 workers was assembled from records of the International Union of Bricklayers and Allied Craftworkers (IUBAC). Mortality was ascertained by linkage to the Canadian Mortality Registry at Statistics Canada. Standardized Mortality Ratios (SMRs) were computed using Ontario general population mortality rates as the reference. RESULTS: Twenty or more years from first membership, SMRs for lung (158; 130-190) and stomach (235; 140-370) cancers were significantly elevated. There were four deaths from pneumoconiosis, but non-malignant respiratory mortality SMRs were not increased. CONCLUSIONS: Bricklayers and Allied Craftworkers are at risk from diseases associated with heavy exposure to inorganic dust: lung cancer, stomach cancer, and pneumoconiosis. Dust control as well as education and training of these workers to protect themselves against inhalation hazards is necessary.