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