1357Journal of Environmental Protection and Ecology 13 , No 3, 13571365 (2012) [607028]

1357Journal of Environmental Protection and Ecology 13 , No 3, 1357–1365 (2012)
Risk assessment
* For correspondence.cheMical air POllUtiOn and the Prev alence Of
resPirat Ory disOrders and diseases
GH. VOICUa, a. BECHIRb, O.-C. aRGHIRb*
aPneumology Hospital of Constanta, Constanta, Romania
b‘Titu Maiorescu’ University of Bucharest, Bucharest, Romania
E-mail: [anonimizat]
abstract. Considering that a given environmental chronical exposure to chemical substances used
in oil industry may influence the risk of occupational respiratory pathology, our study proposed to assign the prevalence of respiratory disorders and diseases in oil company workers from an eastern Romanian region, by using a simplified questionnaire. Method of sampling and randomised selection in 3020 participants included every the 14-th case from the workers in data base. The prevalence study, conducted from 01.01.2000–28.11.2003, included 323 subjects (187 females and 136 males) mean aged 39.4 y.o. +/– 7.136 s.d. (lim: 24–52 years), having a mean perriod of exposure of 12.4 years +/– 7.253 s.d. (lim: 1–32 years). all randomised individuals having respiratory symptoms (n=205),
performed lung function test. Those workers exposed or not to direct chemical air pollution with the best forced expiratory volume in one second (FEV1) < 80% of predicted value were selected. The prevalence of respiratory diseases and disorders among symptomatic workers was increased in both groups of workers exposed or not (111/132; 84.09% versus 52/73; 71.23%; p<0.03). Chemical
air pollution in oil company workers revealed a strong work-exposure related chronic obstructive pulmonary disease (COPD) among nonsmokers and active smokers (p<0.00003) and an increased risk of bronchial asthma as time of exposure becomes longer than 20 years ( p < 0.002).
Keywords: chemical pollution, occupational respiratory pathology, oil company, COPD, bronchial asthma.
aIMS anD BaCKGROUnD
Occupational exposure can affect any organ, and disorders caused by such an
exposure often masquerade as common ailments1. Occupational and other envi-
ronmental factors are significant causes of respiratory diseases and disorders. A survey conducted by american College and Chest Physicians (aCCP) members
revealed 3 major categories of possible occupational and environmental respiratory diseases (OERD) such as pulmonary fibrosis, asthma and rhinitis
2.
Considering that a given environmental chronic exposure to chemical sub-
stances used in oil industry, meaning organic solvents: aliphatic and aromatic hydrocarbons, petroleum solvents, acids, breathable dust which may influence the risk of asthma or other respiratory disease, our study proposed to assign the

1358prevalence of these respiratory disorders among 3094 workers, in an oil company
from a south-eastern Romanian region.
EXPERIMEnT aL
The prevalence study was conducted from 01.01.2000–28.11.2003, by using a
simplified questionnaire inspired by the European Community Respiratory Health Survey (ECRHS) screening questionnaire.
Obtaining the occupational history was considered to be the first goal, con-
sisting in a two-part process of a few routine questions in order to screen for sug-gestive associations between the pattern of
work and the patient respiratory signs
and symptoms. Suspected persons were interrogated with more detailed follow-up
questionning and if the answers arouse clinical suspicion then radiological and ventilatory function tests were recommended. 16 workers with family or personal history of asthma and/or hypersensitivity pathology were excluded as well as 27 workers having a job exposure less than 1 year, because the amount of time spent in the workspace was considered to be an important component of an individual environmental exposure. Sampling and randomised selection of workers included every the 14-th case from original data base. all randomised individuals having
different respiratory symptoms (attacks of cough, prolonged cough, breathless-ness associated or not with wheezing, chest tightness) (n=205), performed lung function tests (3 serial and consecutive tests) with a Flow Screen jaeger device,
determining vital capacity (VC); forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), peak expiratory flow (PEF), maximum expiratory flow at
50% of vital flow capacity (MEF50), maximum expiratory flow at 25% of vital flow capacity (MEF25) +/– bronchodilator test. Those workers exposed or not to direct chemical air pollution with the best FEV1 decreased below 80% of predicted value were selected. analysis was performed using FEV1 as a continuous variable,
according to the severity of respiratory disease mentioned in the contemporary guides of the time (ex. for bronchial asthma national Heart, Lung, and Blood
Institute (nHLBI), World Health Organisation (WHO) report 1995 (Ref. 3). a
potential association between respiratory disease and the period of occupational exposure was determined.
RESULTS
The prevalence study included 323 subjects (187 females and 136 males) mean
aged 39.4 y.o. +/– 7.136 s.d. (lim: 24–52 years), having a mean period of exposure of 12.4 years +/– 7.253 s.d. (lim: 1–32 years) (Table 1).

1359table 1. General characteristics of randomised persons grouped by direct exposure to chemical air
polution
Characteristics Exposed
(E)non-exposed
(nE)Total
(E+nE)
number % number % number %
Categories of age 21–30 yrs 30 14.90 6 50.00 36 11.15
31–40 yrs 96 47.50 42 34.70 138 42.72
41–50 yrs 72 35.60 68 56.20 140 43.34
51–60 yrs 4 20.00 5 4.10 9 2.79
Mean age +/-S.D.
Limits38.07+/–6.613
(24–56 yrs)41.7+/–7.421
(28–56 yrs)39.43 +/–7.136
(24–56 yrs)
Gender females 85 42.10 102 84.30 187 57.89
males 117 57.90 19 15.70 136 42.11
Categories of expo –
sure time < 5 yrs 49 24.30 33 27.30 82 25.39
6–10 yrs 28 13.90 18 14.90 46 14.24
91E+ 41nE = 132 11–15 yrs 63 31.20 23 190.00 86 26.63
16–20 yrs 37 18.30 22 18.20 59 18.27
24E+22nE = 46 21–25 yrs 19 9.40 21 17.40 40 12.38
26–30 yrs 5 2.50 1 0.80 6 1.86
> 30 yrs 1 0.50 3 2.50 4 1.24
Mean time of expo –
sure to environmen –
tal and chemical air pollution (limits)12.40+/– 6.712
(1–30 yrs)12.41 +/– 8.104
(1–32 yrs)12.41+/– 7.253
(1–32 yrs)
Smoking current smo kers 93 46.04 44 35.77 137 42.41
former smokers 50 24.75 27 21.95 77 23.84
non-smok-ers 59 29.21 50 40.65 109 33.75
The frequency of respiratory symptoms was higher than expected, 63.47% (n
= 205/323), being significantly increased in the group of directly exposed workers to chemical air pollution (n=202). 65.35% of all exposed workers to chemical air pollution were symptomatic (‘E’ = 132/202) versus 60.33% in non-exposed (‘NE’ = 73/121) (χ
2 = 0.18; p < 0.7; OR = 1.08; RR = 1.05).
Exposure to all chemical substances used in oil industry produced a wide
range of symptoms from a runny nose and scratchy throat, to bronchitis, persistent cough, dyspnea. Part of exposed worker develops unusual symptoms after switch-ing to a new job but most of the workers recognised to have respiratory problems of breathing and persistent cough after being at a particular job for a while.

1360after pulmonary function testing performed by all symptomatic workers
directly exposed or not to chemical substances, a work-related disorder could be
analysed. In addition, it was considered à priori that if someone develops asthma for the first time as an adult, it could be related to something at their job. Asthma symptoms included frequently wheezing, a persistent dry cough or trouble breath –
ing. COPD is another condition that can develop as a long-term broncho-pulmonary complication after exposure to workplace dangers. Workers exposed for more
than 10 years showed decreased FEV1 and FEV1/FVC ratio. Symptoms include
cough, fatigue, chest tightness and difficulty breathing. A person with bronchitis had a persistent cough that produces mucus or sputum and lasts at least 3 months
to a year.
Most occupational respiratory illnesses were diagnosed on
the basis of the
history, physical examination, chest X-ray film, and, as disorders, were diagnosed
mainly by pulmonary-function tests. an effective approach was firstly to deter –
mine the appropiate diagnosis and then to corelate with the occupational history
to identify possible causes (exposed or not) (Table 2).
table 2. Prevalence of respiratory diseases and disorders among workers
Disease Chemical air pollution PR*
E/nEGender PR*
F/M exposed non-exposed females males
num-
ber% num-
ber% num-
ber% num-
ber%
Rhinosinusitis 6833.90 4738.80 0.87 7339.20 4230.80 1.27
Chronic bronchitis 5426.70 97.40 3.61 2815.00 3525.70 0.58
Bronchoectasis 73.50 1310.70 0.33 13 7.00 75.10 1.37
COPD 14 6.90 32.50 2.76 94.80 85.90 0.81
Bronchial asthma 10 5.00 75.80 0.86 13 7.00 42.90 2.41
Recurrent respiratory
infections10 5.00 75.80 0.86 94.80 85.90 0.81
Distal obstructive syn –
drom (*)73.50 21.70 2.06 63.20 32.20 1.45
Diseases and disorders
(*)111 55.00 5243.00 1.28 9148.70 72 5.90 092
*PR – prevalence report of diseases.
The prevalence of respiratory diseases in directly exposed workers (n ‘E’ =
202) was increased (94/143 versus disorders 7/59; OR=6.84; RR=5.06; CI95%; χ
2 = 27.77; p < 0.0001). The prevalence of respiratory diseases and disorders
among symptomatic workers was increased in both groups of workers (n ‘E’ = 111/132; 84.09% versus 52/73; 71.23 OR = 2.13; RR = 1.18; CI 95%; χ
2 = 4.75;
p < 0.03) (Fig. 1).

1361
fig. 1. Prevalence of respiratory diseases and disorders among symptomatic workers (n = 163/205;
79.51%)
Rhinosinusitis was the most frequent disease diagnosed both in exposed
workers or not (Table 2).
The prevalence of COPD (including chronic bronchitis) was significantly high-
er in exposed workers group (68/202 versus 12/121; OR=3.39; RR=2.79;CI95%;
χ2 = 0.18; p < 0.0002) (Table 2, Fig. 1).
The prevalence of COPD related to smoking was determined among directly
exposed workers to chemical air polution (‘E’) versus non-exposed ones (‘NE’) and the values were 3 times higher in the group of exposed individuals active smokers (48/93; 51.6% versus 6/44; 13.63%; OR=6.76; 2.43<OR<19.76; CI95%; RR=3.78; 1.75<RR<8.17; χ
2=17.91; p<0.00003) and also in non-smokers (8/59;
13.5% versus 2/50; 4%) (Fig. 2).
fig. 2. Prevalence of COPD related to smoking in directly exposed chemical air pollution workers
(E) versus non-exposed (nE)
In the study, forced expiratory volume in 1 s (FEV1) presented different abso-
lute values (mean+/–S.D.) in asthmatics group ( n=17 cases) versus in non-asthmat-
ics (n=188 cases) (2.1 +/–0.9; 66.7+/–12.1 versus 3.0 +/–0.8; 93.7%+/–18.0).

1362Bronchial asthma was diagnosed in 8.29% of symptomatic workers ( n =
17/205); being 2 times more frequent in females (13/187; 6.9%) than in males
(4/136; 2.9%)( χ2 = 2.53; p < 0.2) (Table 2). No significant excess in asthma
prevalence was observed in exposed symptomatic workers (10/202; 4.95%) versus non-exposed ones (7/121; 5.78%) (χ
2 = 0.106; p < 0.8) (Table 2).
asthmatic responses to chemical and dust exposure was different: immediate
(occurring within 2 h after exposure), delayed (4 to 12 h after exposure), or both, but
after asthma diagnosis was established, the symptoms remained constant. Episodes
with increasing severity of symptoms were considered to be very suggestive of an
immunologic sensitisation to an exposure substance.
Tobacco consumption (12/112 versus 5/109) was irrelevant in occupational
asthma (OR=2.3; RR=2.2; χ2 = 2.5; p < 0.2). The prevalence rate of asthma was
greater in former smokers (9/77; 11.6%) than in active (3/35; 8.2%) and non-smokers (5/109; 4.5%) (χ
2 = 2.65; p < 0.2), revealing that occupational exposure
to chemical air pollution could be a major risk factor of illness.
The risk of occupational asthma is influenced only by job exposure time; grow-
ing significantly after 20 years of exposure (Fig. 3). The prevalence of bronchial asthma in workers with occupational history more than 20 years was 4 times higher than the rest (8/57; 14.03% versus 9/266; 3.38%; χ
2 = 10.65; p<0.002).
fig. 3. Prevalence of bronchial asthma related with exposure cumulated time
DISCUSSIOn
The presence of several risk factors, both occupational and non-occupational,
environmental outdoor pollution, can contribute to the development of diseases.
In the general population, an increased risk of rhinosinusitis is associated with a
family history and previous allergic disease. Occupational rhinitis is distinguished
from perennial and seasonal rhinitis by an improvement in symptoms when the
person is away from work. Some people have enhanced responses to environmental
tobacco smoke and other substances4. non-irritant rhinorrhea occurs with cold
air, exposure to cholinergic substances, or exposure to cholinesterase-inhibiting
substances5. allergic occupational rhinitis often precedes occupational asthma but
no worker related sugestive symptoms.

1363We consider that the effects of past and present workplace exposure on a pa-
tient health could be revealed by a simplified ECRHS screening questionning. In
many practices, patients complete health questionnaires before seeing the physi-
cian, but few of these surveys systematically collect information about the patient
work history and history of exposure. By adding questions to such a questionnaire,
the clinician can obtain reliable and valid information on occupational exposure
without sacrificing time spent with the patient6. Even when asked, exposed workers
frequently underestimated the extent of chemical exposure or neglect to tell the
physician about critical work processes that may entail risk7. It was observed that
this happened frequenly and both employees and employers may be misinformed or
unaware of chemical names and toxic effects7. The question ‘do you have asthma?’
was considered to be very specific but, finally, we concluded that question on breathlessness compared to the measurements of lung function, FEV1<80% in particular, provided a better validity.
Most occupational respiratory diseases and disorders are diagnosed on
the basis
of the history, physical examination, chest X-ray film, and pulmonary-function
tests but, firstly, is important to determine the disease pattern and then to use the occupational
history to identify possible causes.
Higher-risk workplaces in oil industry are those with obvious dust, smoke, or
vapour, or fumes of polymers. Soluble gases used in oil industry could be absorbed by the upper-airway mucosa, whereas
less soluble gases penetrate to the alveoli.
The location of particle deposition in the airways is determined by the concen –
tration and size of the particles. Particles that are 10 µm or more in diameter are
deposited in the nose and pharynx, whereas particles that are 5 µm in diameter or
smaller may penetrate to the alveoli. Particles of intermediate size are deposited
in differing proportions at intervening levels. Heavier chemical exposure occurs when there is friction,
grinding, heat, or blasting, when very small particles are
generated, and in enclosed spaces. Main air pollutant emissions are considered to
be sulphur dioxide, nitrogen oxides, carbon monoxide, hydrocarbons, as well as solid particles (dust and carbon ash)
8.
Higher-risk workplaces were defined those where workers are exposed to
obvious dust, smoke, or vapour of organic solvents in heated enclosed area. So,
heavier exposure occurred when very small chemical particles were generated in enclosed spaces. The association of the illness with
work was suspected by a
previous history of symptomatic improvement on weekends or vacations, followed
by increased symptoms on return to work. The pattern of the onset of an identified
respiratory disease after more than 1 year new job started or after a new material
was introduced at the workplace was very suggestive.
The association of the illness with work was suggested especially by a history
of symptomatic improvement on weekends or vacations, followed by increased
symptoms on return to work; it can also be suggested by the onset of disease after

1364a new job is started or after a new material is introduced at the workplace. Strong
chemical irritants (such as ammonia) produce an aversive response, whereas ma-
terials with little sensory effect (such as dust, mist) can be inhaled for prolonged
periods and result in serious injury. Depending on the type of exposure, solutions
can include more ventilation as well as changes in work practices and/or machin –
ery. It is also important that anyone who is concerned about lung exposure quit smoking if they have not already done so.
asthma and chronic obstructive pulmonary disease (both primarily chronic
bronchitis and emphysema) are well-known diseases of the lung airways. CDC consideres both diseases can be brought on by occupational exposure to chemi –
cal substances such as irritants in the workplace. In addition, many workers are unaware that pre-existing asthma and COPD may be worsened by the work envi-ronment. Gases such as formaldehyde, ammonia and chlorine, are found in jobs where chemical reactions occur and in jobs with high heat operations. Vapours can be given off by solvents, and usually irritate the nose and throat first, before they affect the lungs. acids and solvents can also cause damage to the airways.
Latex allergies have become a major problem for healthcare workers, as a result of increased use of protective gloves.
according to the Centers for Disease Control and Prevention (CDC), occu-
pationally related respiratory diseases, including asthma and chronic obstructive pulmonary disease (COPD), pose a significant public health threat
3,7. CDC says that
30% of COPD and adult asthma may be attributable to occupational exposure and more than 20 million US workers are exposed to substances that can cause airway diseases
7. Cigarette smoking is the most common cause of bronchitis, COPD but
workplace exposure factors can also play a role4. So, tobacco consumption could
be a bias for occupational COPD diagnosis but the differences between active smokers with and without directly exposure to chemical air polution revealed an excess of cases statistically significant.
Occupational diseases are preventable. The recognition of occupational causes

can be made difficult by delayed responses that occur at home after work and by
years of latency between exposure in the workplace and the occurrence of disease5,7.
a missed diagnosis means a lost opportunity for meaningful clinical intervention.
From a broader public health perspective, each patient with a work-related illness
represents a ‘sentinel health event’, whose recognition could lead to disease pre-vention if the case
is traced back to the workplace hazards that caused it.
From an economic perspective, there is a growing air pollution generated by
a great variety of production processes8,9, and the failure to prevent occupational
disease results in costly, unnecessary health care after the fact7.

1365COnCLUSIOnS
Environmental and chemical air pollution in an oil company workers revealed a
strong work-exposure related COPD among nonsmokers and active smokers (3
times greater in exposed group workers) and an increasing risk of developping bronchial asthma as time of exposure becomes longer (more than 20 years).
EPIDEMIOLOGICaL IMPLICa TIOnS
Prevalence surveys of occupational disorders are useful for the study of work-forces exposed to chemical air pollution with newly or older recognised agents and mostly in countries where occupationally related respiratory diseases and the circumstances in which they occur are not well recognised. Taking an occupational and environmental history is the single most useful tool in determining weather a respiratory symptom may be related to a disease and to an exposure.
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Received 15 December 2010
Revised 26 January 2011