More Research Needed Review in 2011

1. Atherosclerotic cardiovascular disease

Atherosclerosis is clinically silent as arterial intimal plaques develop over years and decades. Atherosclerosis is the underlying cause in approximately 90% of myocardial infarctions, 60% of strokes, most cases of heart failure, and up to one third of all cases of dementia. Established risk factors for coronary artery disease and stroke are hypertension, diabetes, dyslipidemia, smoking, obesity, physical inactivity, kidney dysfunction, left ventricular hypertrophy, alcohol, and atrial fibrillation. [Cecil, p. 409; 257] "The lifetime risk of coronary artery disease after age 40 is 49% in men and 32% in women. The percentage of cases that are occupationally related is not known." Carbon monoxide (CO) and solvents may trigger ischemia in workers with underlying atherosclerosis. Good evidence associates CO, carbon disulfide, and nitrates with ischemic heart disease IHD), while strong evidence associates exposure to PM2.5 in air pollution with cardiovascular morbidity and mortality. The evidence associating stress, noise, lead, and arsenic with IHD is limited. [APHA, p. 291] "In conclusion, occupational PM [particulate matter] exposure may be associated with IHD mortality and MI. There is also evidence that occupational PM exposure is associated with decreased heart rate variability, a risk factor for CVD mortality and which may be a potential mechanism of PM-associated adverse cardiovascular events and stronger evidence across study cohorts of an association with systemic inflammation, also a potential mechanism of PM-associated IHD. Though data is currently lacking to determine causality, findings from this review justify a greater recognition of the risk of both the development and aggravation of CVD from occupational exposure to PM." [Reference #1] "Whether atherosclerosis is accelerated at levels of carbon monoxide commonly encountered in the workplace is unclear." [LaDou, p. 336] Mean black smoke concentrations fell by 35 ug/m3 after a 1990 ban on sale of coal in Dublin, Ireland. Cardiovascular deaths fell about 10% after this intervention comparing rates in the 3 years before and after the ban. [PMID 12401247] In Ireland, the 98th percentile limit for black smoke (BS) was 250 ug/m3. In 2005 when average levels of BS were below 20 ug/m3, the BS limit was replaced with a PM10 daily mean limit of 50 ug/m3. [www.epa.ie] "With reference to morbidity from respiratory and cardiovascular diseases, European studies in adults do not provide consistent evidence of an association between PM exposure and chronic bronchitis or asthma, nor cardiovascular conditions. Studies on PM10 and lung function, on the other hand, reported positive results." [PMID 19995424] See "Particulate matter." See "Carbon disulfide, chronic toxic effect."

Reference #1: A systematic review of occupational exposure to particulate matter and cardiovascular disease.

Diagnostic: In the Framingham Heart Study, major risk factors were total cholesterol ≥240 mg/dL, systolic pressure ≥160 mmHg, diastolic pressure ≥100 mmHg, smoking, and diabetes. Exercise testing may enhance the predictive value. [UpToDate: Estimation of CV Risk]

Linked to Agents: No established human causal agent (occupational)

2. Hypertension

  1. "Many authorities now question the existence, or at least the clinical significance, of any inherent hypertensive effect of lead beyond that secondarily attributable to lead-associated chronic renal insufficiency." [Rosenstock, p. 583]

  2. "Hypertension is associated with acute lead intoxication, but the relationship between chronic lead exposure and hypertension remains controversial in the setting of mounting evidence." [LaDou, p. 368]

  3. "Increased blood lead levels have been associated with high blood pressure: A doubling of the lead level even within normal limits raises blood pressure 1-2 mm Hg." [APHA, p. 275]

  4. "Lead exposure at the intensity studied (<l.45 micromol/L [<30 microgram/dL]) was not consistently associated with increased conventional or 24-hour blood pressure in the general population or with increased risk of hypertension. These findings argue against the hypothesis that current lead exposure levels are associated with excess cardiovascular morbidity and mortality caused by hypertension." [PMID 8622247]

  5. "In conclusion, there is no consistent relationship between blood pressure and blood lead in the NHANES III dateset." [PMID 12149662]

  6. "In 90 to 95% of hypertensive patients, a single reversible cause of the elevated blood pressure cannot be identified, hence the term primary hypertension. However, in most patients with primary hypertension, readily identifiable behaviors--habitually excessive consumption of calories, salt, or alcohol--contribute to the elevated blood pressure. In the remaining 5 to 10%, a more discrete mechanism can be identified, and the condition is termed secondary or identifiable hypertension." The authors list in table 67-4 the identifiable cause of hypertension: chronic kidney disease; renovascular disease, coarctation of the aorta; primary aldosteronism; Cushing's syndrome; pheochromocytoma; and obstructive sleep apnea. They show the following clinical clues to chronic kidney disease: estimated GFR <60 mL/min/1.73 m2 and urine albumin-to-creatinine ratio >30 mg/g. [Cecil, p. 375]

So, in some groups studied but not all, individuals with higher blood levels of lead had slightly higher blood pressures. A blood pressure elevation of one point does not equate with hypertension. Many of the studies did not control for the risk factors identified in "f" above, e.g., diet, cigarette smoking, and alcohol consumption. Staessen, Roels, and Fagard did control for these factors in the study quoted in "d." "In all analytic studies, particularly observational case-control and cohort designs, confounding must always be considered as an alternative explanation for study findings." (Henneckens, p. 321)

Chronic lead poisoning can cause chronic kidney disease, and chronic kidney disease can cause hypertension.

If a worker had evidence of chronic lead poisoning (elevated blood leads for years) and chronic kidney disease (see the "clinical clues" in "f" above), that would support a diagnosis of hypertension caused by lead-induced chronic renal failure. Otherwise, hypertension, which affects one fourth of the adult population and 70 million Americans, is not an occupational disease.

Diagnostic: "Hypertension has been defined as a usual blood pressure of 140/90 mm Hg or higher." [Cecil, p. 373]

Linked to Agents: No established human causal agent (occupational)

3. Porphyria cutanea tarda

Porphyria cutanea tarda (PCT) is most known for an outbreak of environmental (not occupational) disease in Turkey from 1955 to 1958 when more than 4000 people developed PCT about six months after eating wheat contaminated with the fungicide hexachlorobenzene. There are several other substances associated with disturbance of porphyrin metabolism in humans: 2,4-dichorophenol, 2,4,5-trichlorophenol, 2,3,7,8-tetrachlorodibenzo-p-dioxin, o-benzyl-p-dichlorophenol, 2-benzyl-p-dichlorphenol, vinyl chloride, lead, and aluminum. The two disinfectants (o-benzyl-p-dichlorophenol, 2-benzyl-p-dichlorphenol) were implicated in one case of acquired PCT. Aluminum used in dialysis solutions was thought to be the causal agent in cases of a PCT-like syndrome in patients with renal failure. Workers in polyvinyl chloride production had elevated urinary coproporphyrin levels compared to controls. [LaDou, p. 214] "People with metabolic disorders associated with the synthesis of porphyrins (important intermediates in the synthesis of hemoglobin, cytochromes, and vitamin B12), collectively known as porphyrias, are especially susceptible to lead exposure since lead inhibits two critical enzymes, ALAD and ferrochelatase, concerned with heme synthesis in erythrocytes." [ATSDR ToxProfiles: Lead]

In another chapter in LaDou, the authors write, "2,3,7,8-TCDD may inhibit uroporphyrinogen decarboxylation, and cases of porphyria cutanea tarda among exposed workers have been reported. However, recent studies have failed to find an association between 2,3,7,8-TCDD and porphyrin levels. No association has been observed among former chlorophenol production workers between 2,3,7,8-TCDD exposure and serum transaminase levels, induction of cytochrome P450 activity, peripheral neuropathy, chronic bronchitis or chronic obstructive pulmonary disease, and porphyria cutanea tarda." [LaDou, p. 476]

According to Cecil Medicine, 24th edition, "Porphyrias are due to deficiencies of specific enzymes of the heme biosynthetic pathway and, when clinically expressed, are associated with striking accumulations of heme pathway intermediates. Porphyria cutanea tarda (PCT) , the most common of these disorders, is primarily an acquired, iron-related disorder. The others occur only with mutations of an enzyme in the heme biosynthetic pathway." Table 217-1 in Cecil shows that PCT is inherited as an autosomal dominant disease. The presenting symptoms are blistering skin lesions. Exacerbating factors are iron, alcohol, estrogens, hepatitis C virus, and halogenated hydrocarbons. The most important screening test is plasma or urine porphyrins, and treatment is with phlebotomy or low-dose hydroxychloroquine. [Cecil, p. 1363-71]

"Porphyria cutanea tarda seems to be a disease in which symptoms develop when residual hepatic uropophyrinogen decarboxylase decrease below a threshold of about 25%. The risk factors that contribute to inactivation or inhibition of this enzyme are mainly alcohol abuse, oestrogeens, hepatitis C, and to a lesser extent HIV infections and genetic haemochromatosis. These precipitating factors act either alone or in combination with hepatic iron overload, an almost universal finding in porphyria cutanea tarda, to generate an iron-dependent oxidative mechanism." [PMID 20226990]

Environmental chemical exposures and disturbances of heme synthesis.

Diagnostic: Initial screening test: plasma and urine porphyrins;

Linked to Agents: No established human causal agent (occupational)

4. Rheumatoid arthritis

Rheumatoid arthritis (RA) has been associated with silicosis in a number of studies. [Rom, p. 379] "Although RA involves autoimmune reactions, the precise cause is unknown; many factors may contribute. . . . Unknown environmental factors (e.g., viral infections) are thought to play a role.." [Merck Manual, p. 283] RA is 2-3 times more prevalent in women than in men. "Despite the absence of clear evidence linking any infectious agent to RA, it is widely believed that ultimately an important triggering role will be elucidated for infectious or other environmental agents." [Cecil, p. 1682-3] 1,022 cases of silicosis were reported in the state of Michigan between 1985 to 2006, Medical records were available for 790 of these cases and showed a diagnosis of rheumatoid arthritis in 33 (a prevalence ratio of 2.26, or 6.96, depending upon the reference rate used). [PMID : 20957678] In a study of autoimmune disease mortality in 26 US states and occupational exposures, no increased risk of RA was found for those in jobs likely to include exposure silica. [PMID 17907164] Silicosis affects the immune system; patients have increased susceptibility to tuberculosis and other infections, but silicosis does not cause TB. [LaDou, p. 327]

Diagnostic: Must have 4: 1.) Morning stiffness >1 h; 2.) Arthritis > 2 joints; 3.) Hand affected (wrist, MP or PIP); 4.) Symmetric arthritis; 5.) Rheumatoid nodules; 6.) Rheumatoid factor +; 7.) Typical x-ray changes; [Merck Manual, p. 284]

Linked to Agents: No established human causal agent (occupational)

5. Scleroderma

Scleroderma has been associated with silicosis in a number of studies. [Rom, p. 379] 1,022 cases of silicosis were reported in the state of Michigan between 1985 to 2006, Medical records were available for 790 cases and showed a diagnosis of scleroderma in two (a prevalence ratio of 28.3). [PMID: 20957678] Silicosis affects the immune system; patients have increased susceptibility to tuberculosis and other infections, but silicosis does not cause TB. [LaDou, p. 327] "Because some SSc autoantibodies cross-react with certain virus-associated epitopes, molecular mimicry has been considered a possible pathogenetic link between viral infection and SSC." [Cecil, p. 1706] The female-to-male ratio of patients with SSc is about 4:1. [Merck Manual, p. 270] In a study of autoimmune disease mortality in 26 US states and occupational exposures, no increased risk of scleroderma was found for those in jobs likely to include exposure to silica or solvents. [PMID 17907164] "Immunologic mechanisms and heredity (certain HLA subtypes) play a role in etiology. SSc-like syndromes can result from exposure to vinyl chloride, bleomycin, pentazocine, epoxy and aromatic hydrocarbons, contaminated rapeseed oil, or L-tryptophan." [Merck Manual] The results of this meta-analysis suggest that silica exposure is associated with increased risk for the development of SSc and specifically in males. However, the evidence to date is not sufficient to conclude that silica  is a causative factor for SSc." [PMID 20047060] A number of scleroderma-like disorders after occupational or environmental exposures have been reported. For the disease caused by vinyl chloride, see "Acroosteolysis." "Toxic oil syndrome" affected thousands in Spain in 1981 after ingestion of cooking oil contaminated with aromatic amines. In 1989 an epidemic of eosinophilia-myalgia syndrome occurred after consumers ingested an L-tryptophan remedy contaminated with aromatic amines.. [Rosenstock, p. 537-8]

Diagnostic: Suspected in patients with Raynaud's phenomenon, dysphagia, and tight skin with + ANA (present in 90% often with an antinucleolar pattern) and + rheumatoid factor (present in 33%); [Merck Manual, p. 271]

Linked to Agents: No established human causal agent (occupational)

6. Solvent-induced hearing loss

Noise-induced hearing loss was listed in 1991 as one of the 64 sentinel health events that cause preventable disease and disability in workers. [Mullan, p. 782] In recent years, concern has been raised about the impact of organic solvents such as toluene and styrene on occupational hearing loss. "While the ototoxicity of both solvents is clearly demonstrated in rat studies, their ototoxic potency in humans is not well characterised yet." The rat experiments showed a NOAEL of about 300 ppm for styrene and about 1000 ppm for toluene. The current workplace limits are 20 ppm for both styrene and toluene, and the IDLH levels are 700 ppm and 500 ppm respectively. [PMID 18259983] "On the whole, studies on employees in various branches of industry gave inconsistent results. Indeed, a clear relationship between solvent and hearing impaiment is difficult to assess with epidemiological studies . . . " [See Hyperlink] "Due to missing toluene effects, it was concluded that the threshold level for developing hearing loss as a result of occupational exposure to toluene plus noise might be above the current limit of 50 ppm toluene." [PMID 19042192] In a review published by IRSST, only four chemicals (lead, styrene, toluene, and trichloroethylene) were designated as "ototoxic substance." Of these four, only lead had "evidence of interaction" with noise. [www.irsst.qc.ca] See "Noise-induced hearing loss."

Hyperlink: EU-OSHA: Combined exposure to noise and ototoxic substances

Audiogram: graphs the softest sounds that the subject can hear as a function of frequency;

Linked to Agents: No established human causal agent (occupational)

7. Noise-induced hearing loss

Presbycusis (sensorineural hearing loss in older people) results mainly from aging and noise exposure. Prevalence rates of presbycusis are 25% to 40% in people >65 and 40% to 66% in those >75. [Merck Manual, p. 781-3] Noise-induced hearing loss (NIHL)  was listed in 1991 as one of the 64 sentinel health events that cause preventable disease and disability in workers. [Mullan, p. 782] In recent years, concern has been raised about the impact of organic solvents such as toluene and styrene on occupational hearing loss. See "Solvent-induced hearing loss." In a review published by IRSST, only four chemicals (lead, styrene, toluene, and trichloroethylene) were designated as "ototoxic substance." Of these four, only lead had "evidence of interaction" with noise. [www.irsst.qc.ca] In a review of "occupational exposure to chemicals and hearing impairment," the Nordic Expert Group found a blood lead NOAEL of 35ug/dl and a LOAEL of 55 ug/dl in long-term exposed monkeys. Interaction of lead poisoning with noise has not been studied in animals. "In humans, central auditory effects have been associated with current exposures and life-time weighted average blood lead concentrations of approximately 28-57 ug/dl." [Hyperlink] CDC statistics on blood lead reporting in 40 states showed a decline in the prevalence of blood leads >25 ug/dl from 14 per 100,000 employed adults in 1994 to 6.3 per 100,000 in 2009. [MMWR Weekly, July 1, 2011] The mean blood lead in the US has declined from about 15 ug/dl in the 1970s when leaded gasoline was used to the current level of <2 ug/dl. [Levy, p. 203] OSHA regulates noise exposures at or above an 8-hour time-weighted average of 85 dBA; [LaDou, p. 115] "Exposure to certain chemicals may also result in hearing loss. In settings where there may be exposures to noise and to carbon monoxide, lead, manganese, styrene, toluene, or xylene, periodic audiograms are advised and should be carefully examined." [ACGIH: TLVs and BEIs]

Hyperlink: Nordic Expert Group: Occupational exposure to chemicals and hearing impairment

Diagnostic: Audiogram: graphs the softest sounds that the subject can hear as a function of frequency; NIHL first affects hearing around 4000 Hz; After prolonged or severe exposure, the speech frequencies (500-3000 Hz) are affected; [LaDou, p. 114]

Linked to Agents: Noise

8. Birth defects

Established hazards are exposure to lead, methyl mercury (ingestion), toluene (glue sniffing), alcohol (abuse), glycol ethers, PCBs (ingestion), ionizing radiation, (atomic blast), and heat. [Luderer, p. 634]

Hyperlink: The effect of fever, febrile illnesses, and heat exposures on the risk of neural tube defects in a Texas-Mexico border population.

Linked to Agents: Radiation, ionizing; Mercury, alkyl compounds; GLYCOL ETHERS; and Lead;

9. Infertility, female

Established occupational hazards are toluene, 2-bromopropane, nitrous oxide, antineoplastic drugs (therapeutic uses), ionizing radiation (accidents or radiation therapy), and shift work. [Luderer, p. 631]

Linked to Agents: 2-Bromopropane; Radiation, ionizing; Nitrous oxide; Toluene;

10. Spontaneous abortions

Established risks include medical hazards (antineoplastic drug dispensing, anesthetic gases, nitrous oxides used by dental assistants, and ethylene oxide), lead, ethylene glycol ethers in the semiconductor industry, ingestion of PCBs in food, heavy labor, and shift work. Occupational use of various organic solvents has also been linked to spontaneous abortions. [Luderer, p. 632]

Linked to Agents: GLYCOL ETHERS; WASTE ANESTHETIC GASES; Nitrous oxide; Ethylene oxide; Lead;

11. Noise

Sources/Uses: Noise is the major risk factor for occupational hearing loss. Approximately 30 million US workers are exposed to hazardous noise every year. [PMID 18259983] Most workers exposed to hazardous noise are employed in the manufacturing industries. More than 1/2 of workers in textiles, lumber and wood, and mining are exposed to excess noise. [Wald, p. 279]

Comments: Noise is measured in three main ways: frequency, intensity, and duration. Frequency is measured in cycles per second or hertz (Hz). Humans hear best at 1000 to 5000 Hz. A decibel (dB) is a measure of relative loudness on a logarithmic scale. Workers with daily exposures >85 dB as an 8-hour time weighted average must be covered by a hearing conservation program. [Wald, p. 279-81] The OSHA standard limits workers' exposure to noise: 90 dB (equivalent to the noise of a lawnmower) for 8 hours; 95 dB for 4 hours; 100 dB for 2 hours; [UpToDate]

Linked to Occupational Diseases: Noise-induced hearing loss

12. Particulate matter

Description: Particles smaller than 10 microns are designated PM10 fraction, and those <2.5 microns the PM2.5 fraction (the fine fraction). PM10 passes the larynx (thoracic fraction); PM2.5 reaches the alveoli (respirable fraction); [Levy, p. 532]

Sources/Uses: Natural (forest fires and volcanic eruptions) and related to human activity (anthropogenic); The main sources of PM2.5 are the combustion of fossil fuels (industry, transportation, and power plants) and biomass burning for heating and cooking. [PMID 20458016]

Comments: For fine particulate, US air standards allow 15 ug/m3 annual average and 35 ug/m3 in a 24-hour period. Seventeen percent of US residents live in nonattainment areas for the annual average and 30% in nonattainment areas for the 24-hour standard. [Levy, p. 497] An Air Quality Index (AQI) of 0-50 is considered "Good" with no recommended restriction of athletic practice. An AQI of 0-50 corresponds to a PM2.5 <17.5 ug/m3 and a PM10 <75 ug/m3 as 24 hour averages. [Reference #1] The American Cancer Society (ACS) cohort was used in the most intensive study of air pollution mortality. After a follow-up period averaging eight years, the study of 151 US communities showed that PM2.5, but not PM10, was associated with cardiovascular and lung cancer mortality. Long-term instillation of particulate matter into the airways of rabbits increases coronary atherosclerosis. [Rom, p. 1498-1500]

Reference #1: EPA Air Quality Index (AQI): A Guide to Air Quality and Your Health

Linked to Occupational Diseases: None

13. Diesel exhaust

Sources/Uses: Workers exposed to diesel exhausts include "mine workers, bridge and tunnel workers, railroad workers, loading dock workers, truck drivers, material handling machine operators, farm workers, auto, truck and bus maintenance garage workers, and longshoring employees." [Reference #1] Highest levels occur in underground mining and construction with heavy equipment with elemental carbon (EC) = 27-658 ug/m3; Medium levels occur in enclosed areas with smaller engines such as shop mechanics and dock workers with EC >50 ug/m3; Lowest levels occur in drivers, train crew, surface construction and mining, parking attendants, vehicle testers, utility service workers, and airline ground crew with EC <25 ug/m3;  [PMID 19277070] EC comprises approximately 20% of diesel exhaust respirable particulate matter (PM); Therefore, 5 X EC = PM respirable in ug/m3; [Harber, p. 574]

Comments: "Some experimental evidence and some epidemiologic evidence suggest that emissions from diesel-powered engines may be lung carcinogens, but the epidemiologic evidence is inconclusive." [Siemiatycki, p. 336] Assessment of risk is difficult because of improvements in diesel engines in recent years. [Schottenfeld, p. 364] "Diesel asthma" was documented in three railroad workers who developed reactive airway disease after heavy exposure to locomotive exhaust while riding behind the engine in caboose-less trains. [PMID 8433186] Increased risk of COPD mortality was found in railroad workers exposed to diesel exhaust in the period 1960-1990; [Reference #2] Tunnel workers exposed to nitrogen dioxide from blasting and diesel exhaust had decreased pulmonary function. [PMID 14985522] See "Nitrogen dioxide."

Reference #1: OSHA Technical Links: Diesel Exhaust

Reference #2: Chronic obstructive pulmonary disease mortality in railroad workers.

Linked to Occupational Diseases: Pulmonary disease, chronic obstructive

New high-risk job task: Work for railroad in 1960s or 1970s as engineer, fireman, conductor, brakeman, or hostler

Old high-risk job task: Work in tunnel construction for years with heavy exposure to NO2 (blasting & diesel exhaust)

14. Environmental tobacco smoke

Sources/Uses: Average concentrations of particulate matter (PM2.5) in residences with smokers is 30 ug/m3; [Rom , p. 1394] Average PM2.5 concentrations in casinos are 63 ug/m3, about 9 times higher than concentrations outside; [PMID 20160761]

Comments: Exposure to environmental tobacco smoke (ETS) is associated with lung cancer, cardiovascular disease, and respiratory effects in studies of people who never smoked. [Levy, p. 148] Workers in bars, restaurants, and offices are exposed to environmental tobacco smoke, which is designated by IARC as a Group 1 human carcinogen. [Siemiatycki, p. 327] "The results of both study designs [case control and cohort] may be affected by inaccurate assessment of exposure to SHS, by inaccurate information on personal smoking habits that leads to classification of smokers as nonsmokers, by failure to assess and control for potential confounding factors, and by the misdiagnosis of a cancer at another site as a primary cancer of the lung." [Schottenfeld, p. 374] The best available biomarker for ETS is cotinine. "However, because the half-life for cotinine is about 17 h, it does not provide a valid marker for past ETS exposure. Therefore, unless a prospective study of ETS exposure and lung cancer in non-smokers is being conducted, there is presently no valid and reliable biomarker for past ETS exposure." [PMID 12379877] Average levels of ETS exposure are comparable for home and unregulated work environments, but some bars and restaurants have exceptionally high levels. [PMID 16880370] Producing tumors from cigarette smoke in experimental animals is difficult. "To compensate, the animals are treated with much higher doses of smoke than those humans in real life are usually exposed to. For example, most smoke inhalation studies in rodents administer doses of smoke with an average total particulate matter, which corresponds to a human smoking of 2-4 packs of cigarettes per day. . . . Consequently, although the causal link between SHS [secondhand smoke] exposure and lung cancer development is well-established, the estimated risk for developing lung cancer consequent to SHS exposure remains somewhat debatable." [PMID 18598930] Randomly selected participants from electoral rolls in central Italy included 977 smokers and 2402 nonsmokers. Of the nonsmokers, 882 were exposed to ETS, and 1520 were not, based on self-report. Average serum cotinine levels were 2.8 (ETS nonexposed nonsmokers), 4.4 (ETS exposed nonsmokers), and 277.3 (current smokers). [PMID 12908713] "A recent study on women participating in a prenatal clinic in Philadelphia found that 73% of those who classified themselves as nonsmokers had urinary cotinine values above 80 ng/ml, the cutoff used to distinguish smokers from nonsmokers." [PMID 19125149] The difference was greater than 24% in five studies that compared prevalence estimates of smoking based on self-reported and measured values. [PMID 19246437] The average urinary cotinine levels from hospitalized children aged 3 to 27 months was 0.44 ng/mg creatinine (no exposure), 4.10 (parents smoke outside the house), and 5.30 (parents smoke inside the house). [PMID 11801622]

Linked to Occupational Diseases: Lung cancer

New high-risk job task: Exposed to tobacco smoke working in unregulated bars, restaurants, or casinos

 

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