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Introduction: Increased rates of leukaemia have been found among tanker crews. Occupational exposures to the leukomogen benzene during loading, unloading, and tank cleaning are possible causes. Studies on older types of tankers carrying gasoline with most handling being done manually have revealed important exposures to benzene. Our study explores benzene exposures on tankers with both automatic and manual systems. Correlations between benzene exposure and benzene in alveolar air (AlvBe), benzene in urine (UBe), and trans,trans-muconic acid (ttMA) in urine were investigated., Methods: Forty-three male seafarers (22 deck crewmembers and 21 not on deck) on five Swedish different product and chemical tankers transporting 95- or 98-octane gasoline were investigated between 1995 and 1998. The tankers used closed systems for the loading and unloading of gasoline but stripping and tank cleaning were done manually. Benzene in respiratory air was measured using personal passive dosimeters during a 4-h work shift. Samples for biomarker analyses were collected pre- and post-shift. Smoking did occur and crewmembers did not use any respiratory protection during work., Results: The average 4-h benzene exposure level for exposed was 0.45 mg m-3 and for non-exposed 0.02 mg m-3. Benzene exposure varied with type of work (range 0.02-143 mg m-3). AlvBe, UBe, and ttMA were significantly higher in post-shift samples among exposed and correlated with exposure level (r = 0.89, 0.74, and 0.57, respectively). Smoking did not change the level of significance among exposed., Discussion: Benzene in alveolar air, unmetabolized benzene, and ttMA in urine are potential biomarkers for occupational benzene exposure. Biomarkers were detectable in non-exposed, suggesting benzene exposure even for other work categories on board tankers. Work on tankers carrying gasoline with more or less closed handling of the cargo may still lead to significant benzene exposure for deck crewmembers, and even exceed the Swedish Occupational Exposure Limit (OEL; 8-h time-weighted average [TWA]) of 1.5 mg m-3., (© The Author(s) 2019. Published by Oxford University Press on behalf of the British Occupational Hygiene Society.)

Background: Previous investigations indicate that engine room personnel on ships are exposed to polycyclic aromatic hydrocarbons (PAH) from oil and oil products, with dermal uptake as the major route of exposure. Several PAH are known carcinogens and mutagens., Aims: To investigate the urinary excretion of a marker for oxidative DNA damage, 8-hydroxydeoxy-guanosine (8OHdG), in engine room personnel, and to study the association between 8OHdG and 1-hydroxypyrene (1OHP), a biological marker for PAH exposure., Methods: Urine samples were collected from engine room personnel (n = 36) on 10 Swedish and Norwegian ships and from unexposed controls (n = 34) with similar age and smoking habits. The exposure to oils, engine exhaust, and tobacco smoke 24 hours prior to sampling was estimated from questionnaires. The urinary samples were frozen for later analyses of 8OHdG and 1OHP by high performance liquid chromatography., Results: Excretion in urine of 8OHdG (adjusted to density 1.022) was similar for controls (mean 18.0 nmol/l, n = 33), and for those who had been in the engine room without skin contact with oils (mean 18.7 nmol/l, n = 15). Engine room personnel who reported skin contact with oil had increased excretion of 8OHdG (mean 23.2 nmol/l, n = 19). The difference between this group and the unexposed controls was significant. The urinary levels of ln 1OHP and ln 8OHdG were significantly correlated, and the association was still highly significant when the effects of smoking and age were accounted for in a multiple regression analysis., Conclusion: Results indicate that exposure to PAH or possibly other compounds from skin contact with oils in engine rooms may cause oxidative DNA damage.

Objectives: To investigate the risk of lymphatic and haematopoietic malignancies in deck crew on tankers exposed to cargo vapours., Methods: The study design was as a nested case-referent study in two cohorts of male Swedish seamen 20-64 years of age at the national census 1960 (n 13,449) and 1970 (n 11,290), respectively. Cases were detected by record linkage with the Swedish Cancer Register 1961-79 and 1971-87, respectively. For each case, three to five age matched referents from the population were selected. Exposure was assessed from data in the Swedish Registry of Seamen and from a register of Swedish ships., Results: Seamen in the 1970 cohort, who had been exposed to cargo vapours for at least one month on chemical or product tankers, had an increased risk of lymphatic and haematopoietic malignancies (Mantel-Haenszel odds ratio (OR) 2.6, 95% confidence interval (95% CI) 1.1 to 5.9)) with a significant exposure-response relation (conditional logistic regression analysis, p = 0.04). The ORs were increased for both lymphoma (3.2), multiple myeloma (4.0), and leukaemia (1.6), but the increase was only significant for non-Hodgkin's lymphoma (OR 3.3, 95% CI 1.1 to 10.6). There were no significantly increased risks for the 1960 cohort or for seamen exposed only on crude oil tankers, but these groups had few exposed cases and low cumulative exposure to benzene and other light petroleum products., Conclusions: Seamen exposed to cargo vapours from gasoline and other light petroleum products on chemical or product tankers had an increased incidence of lymphatic and haematopoietic malignancies. One possible cause is exposure to benzene during loading, unloading, and tank cleaning operations.

Objectives: To estimate the risk of cancer due to occupational exposure to petroleum products in the Swedish transport and refinery industries., Methods: In a retrospective cohort study the cancer incidence in 4128 men and 191 women, who had worked for at least one year in the petroleum industry, was compared with the incidence in the general population. The job titles and employment times for each person were found in personal files in the industries. The men had on average worked in jobs exposed to petroleum for 11.6 years at the end of the observation period. The cases of cancer were identified by record linkage with the Swedish cancer register., Results: In total there were 146 cases of cancer v 157.6 expected (standardised mortality ratio (SMR) 0.93 90% confidence interval (90% CI) 0.80 to 1.1). Operators at refineries had an increased risk of leukaemia (6 cases v 1.7 expected, 90% CI of relative risk (RR) 1.5 to 7.0). Five of the six cases had started to work at the refineries in the 1950s or later. No other significantly increased risk of cancer was found. Distribution workers had a decreased incidence of lung cancer (no cases, 90% CI of RR 0 to 0.4)., Conclusions: Operators at Swedish refineries had an increased risk of leukaemia. A possible cause is exposure to benzene. There was no increased risk of leukaemia in distribution workers. Distribution workers had a decreased risk of lung cancer.

Until the introduction of self-service around 1970, service station workers in the Nordic countries were exposed to gasoline vapors. Based on measurements reported in the literature, the 8-hour time-weighted average benzene exposure was estimated to be in the range of 0.5-1 mg/m3. We studied the cancer incidence in a cohort of 19,000 service station workers from Denmark, Norway, Sweden, and Finland. They were identified from the 1970 censuses and followed through 20 years, where 1,300 incident cancers were observed. National incidence rates were used for comparison. The incidence was not increased for leukemia (observed = 28, standardized incidence ratio (SIR) = 0.9, 95% confidence interval (CI) 0.6-1.3) not for acute myeloid leukemia (observed = 13, SIR = 1.3, 95% CI 0.7-2.1). The incidence was slightly elevated for kidney cancer observed = 57, SIR = 1.3, 95% CI 1.0-1.7) and for pharyngeal, laryngeal, and lung cancer. A 3.5-fold risk of nasal cancer was found (observed = 12, SIR = 3.5, 95% CI 1.8-6.1). This cohort exposed to gasoline vapors with benzene levels estimated to be 0.5-1 mg/m3 showed no excess risk of leukemia or acute myeloid leukemia, a 30% elevated risk of kidney cancer, and a previously unnoticed risk of nasal cancer.

Benzene is an established cause of leukemia in adults, especially acute non-lymphocytic leukemia (ANLL). A few studies have indicated that exposure to gasoline is a cause of childhood leukemia. The purpose of this study was to investigate if environmental exposure to benzene from gasoline and car exhaust was associated with leukemia in children and young adults. The exposure to gasoline and car exhaust was estimated by the number of cars per area. In this ecology study, data on the incidence of cancer in each municipality of Sweden during an 11-year period (1975-1985) were compared with the number of cars per area. Data on the incidence of cancer for persons aged 0-24 years at diagnosis were collected from the National Swedish Cancer Register. The following diagnoses were studied: non-Hodgkin's lymphoma, acute lymphocytic leukemia (ALL), chronic myeloid leukemia (CML), and acute myeloid leukemia (AML). We found an association between AML and car density. In municipalities with more than 20 cars/km2 the incidence of AML was 5.5 [95% confidence interval (CI) 4.4-6.8, n = 89] as compared with 3.4 (95% CI 1.9-5.7, n = 15) cases per 1 million person-years in municipalities with less than 5 cars/km2 (P = 0.05). No association was found for the other sites of cancer studied. The association between AML in young adults and car density might be attributable to exposure to benzene from gasoline vapors and exhaust gases, but further investigations are necessary before any definite conclusion can be drawn.

Objective: The deck crew on tankers can be exposed to high concentrations of benzene and other chemicals during loading, unloading and tank-cleaning operations. The objective of this study was to investigate whether genotoxic or other early health effects of cargo vapour exposure could be detected in coastal tanker crews., Methods: The association between exposure to cargo vapours and clinical symptoms and signs, spirometry, blood cell count, blood test for liver function, and the frequency of micronuclei and sister chromatid exchanges in peripheral lymphocytes was studied in a cross-sectional investigation of 107 male crew members (66 deck crew and 41 others) on ten coastal tankers., Results: Seven of the tankers had automatic cargo level gauging systems but some of the ships still had open hatches during loading and unloading operations. Acute symptoms such as headache, nausea, vertigo, fatigue and dizziness after loading or tank-cleaning operations were reported by 56 of the 66 deck crew members (85%). Irritation of the mucous membrane in eyes and upper respiratory tract by cargo vapours were also common in this group. Obstructive symptoms were more common in the group with the highest exposure to cargo vapours but persistent effects on lung function (vital capacity and forced expiratory volume in 1 s), nervous system, liver enzymes or blood counts were not found. The frequency of micronuclei after mitotic stimulation with phytohaemagglutinin was higher among the deck crew (mean 4.2 SEM 0.40) than in other crew members (mean 3.6, SEM 0.35). although the difference was not statistically significant. We found no association between exposure and the frequency of sister chromatid exchanges or micronuclei after stimulation with pokeweed mitogen., Conclusion: This study indicates that exposure to cargo vapours in coastal tanker crews may cause symptoms in the respiratory and nervous systems.

Objective: Machinists have an increased risk of lung cancer and bladder cancer, and this may be caused by exposure to carcinogenic compounds such as asbestos and polycyclic aromatic hydrocarbons (PAHs) in the engine room. The aim of this study was to investigate the exposure of engine room personnel to PAHs, with 1-hydroxypyrene in urine as a biomarker., Methods: Urine samples from engine room personnel (n = 51) on 10 ships arriving in different harbours were collected, as well as urine samples from a similar number of unexposed controls (n = 47) on the same ships. Urinary 1-hydroxypyrene was quantitatively measured by high performance liquid chromatography. The exposure to PAHs was estimated by a questionnaire answered by the engine room personnel. On two ships, air monitoring of PAHs in the engine room was performed at sea. Both personal monitoring and area monitoring were performed. The compounds were analysed by gas chromatography of two types (with a flame ionisation detector and with a mass spectrometer)., Results: Significantly more 1-hydroxypyrene was found in urine of personnel who had been working in the engine room for the past 24 hours, than in that of the unexposed seamen. The highest concentrations of 1-hydroxypyrene were found among engine room personnel who had experienced oil contamination of the skin during their work in the engine room. Stepwise logistic regression analysis showed a significant relation between the concentrations of 1-hydroxypyrene, smoking, and estimated exposure to PAHs. No PAHs were detected in the air samples., Conclusion: Engine room personnel who experience skin exposure to oil and oil products are exposed to PAHs during their work. This indicates that dermal uptake of PAHs is the major route of exposure.

To study genotoxic effects of exposure to low levels of benzene, single-strand breaks (SSB) in DNA of leukocytes and urinary levels of the oxidative DNA adduct 8-hydroxydeoxyguanosine (8OHdG) were determined in 33 men occupationally exposed to benzene from gasoline and in 33 controls. The average exposure to benzene over a shift was determined by personal air sampling in the breathing zone. The 8-hr time-weighted average exposure to benzene was 0.13 ppm (mean value, range 0.003-0.6 ppm). Exposed workers had a significant increase of SSB (p = 0.04) over the shift compared with controls. Storage time of the samples seemed to affect the results. An analysis of samples with the same storage time showed a nonsignificant increase among the workers compared with controls. Urinary 8OHdG increased over the shift among the exposed workers but not among the controls. The highest values among the exposed workers were seen in late evening, with a slight decrease the next morning. Multiple linear analysis adjusting for smoking habits showed a significant association between the exposure level of benzene during the shift and the increase of 8OHdG in the urine over the shift among exposed workers (p = 0.02). These findings indicate a genotoxic effect in humans of benzene at relatively low exposure levels, that is, about 0.1 ppm (0.3 mg/m3).

The purpose of this study was to ascertain whether parental age and parental pre-conceptional exposure to various agents differentiated children with Prader-Willi syndrome (PWS) from obese children without PWS. Two groups of patients under 25 years of age were studied, 15 persons with PWS, and 13 with PWS-like symptoms. In the PWS group deletions were detected on chromosome 15q11-q13 and parents were older. The parents' occupational and recreational exposure to environmental toxins was recorded and correlated to the clinical diagnosis, genetics and behaviour characteristics. Paternal exposure to gasoline/petrol was significantly higher in the PWS group and is suggested as a possible important factor in the aetiology of PWS.

A simple and reliable field method is presented for sampling and analysis of benzene in end-exhaled air. The sample is collected directly on an adsorbent tube while the subject exhales through a sampling device consisting of a modified peak expiratory flow meter. To ensure sampling of end-exhaled air, the temperature of the breath is monitored during expiration. The analytes subsequently are thermally desorbed and analyzed by gas chromatography. No sample preparation before analysis is needed, and therefore sample loss is minimized, shipping is easy, storage is possible, and clean up is unnecessary. All these steps have been major problems in earlier methods for breath analysis. The presented method has been applied to the monitoring of benzene. The separation of benzene from other components of exhaled air was good and the detection limit low (0.5 microgram/m3), and therefore benzene could be monitored in occupationally nonexposed nonsmokers. No carry-over in the sampling device or breakthrough could be detected. The samples were stable for at least a week. The combined precision in sampling and analysis was excellent, with a coefficient of variation of 13%.

A survey was conducted at 15 textile plants with dyehouses in western Sweden. Employees with a history of work related rhinitis, asthma, or skin symptoms were offered a clinical and immunological investigation including skin prick tests, skin patch tests, and radioallergosorbent tests (RASTs) to detect specific allergy to reactive dyes. Among the 1142 employees, 162 were exposed to reactive dyes and 10 of these (6%) reported work related respiratory or nasal symptoms. An allergy to reactive dyes could be confirmed in five (3%, 95% confidence interval 1-7%). All but one had been exposed to reactive dyes for one year or less before the onset of symptoms. Positive RASTs could be detected in four of the five patients. All of the RAST positive patients were positive to remazol black B, but six out of eight additional remazol dyes also elicited positive results. RAST and RAST inhibition showed a cross reactivity between some of the dyes. Seven persons with work related dermatitis and three with urticaria or Quincke oedema were found. In one patient contact dermatitis to a monoazo dye was shown, but no positive patch test reactions to reactive dyes. IgE-mediated allergy to reactive dyes seems to be an important cause of respiratory and nasal symptoms among dyehouse employees exposed to dust from reactive dyes.

Methods of assaying reactive dye-specific IgE antibodies were investigated with a RAST. Sera from three patients, occupationally exposed to a reactive dye, Remazol black B (Chemical Abstract registry number 17095-24-8), were used. Directly dyed disks, that is, disks without any carrier protein, resulted in poor and unreliable measures of specific IgE. In contrast, optimized preparation of conjugates between the dye and human serum albumin resulted in efficient binding of specific IgE. The patients' RAST results were strongly positive, whereas sera from 36 exposed workers but without symptoms and sera from unexposed subjects with high levels of total IgE were negative. The hapten and carrier specificity of the IgE antibodies was studied by direct RAST and RAST inhibition. In one patient, the antibodies were principally hapten specific, whereas another patient was found to have antibodies with a high degree of specificity to the carrier. The third patient's antibodies were intermediate between the other two patients' antibodies in this respect, suggesting that antibody specificity is dependent not only on the nature of the hapten but also on individual immune response factors. The study demonstrates that it is important to use an optimized preparation of dye-protein conjugates to elicit reliable results and a high degree of specific IgE binding in the RAST.

Deck officers on coastal tankers may be exposed to high concentrations of cargo vapors during loading and tank-cleaning operations. Two cases of acute nonlymphatic leukemia are described. Both men had worked as chief officers on coastal tankers transporting benzene and other petroleum products.