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Environmental Pollution | Jindal Chest Clinic
1. Environment
• Surroundings: Conditions of life or
growth
• Air, water, soil, light, sound, vegetation,
forests, animals and micro-organisms
• Outdoor – Indoor
• Home – Work place
• Micro-environments
2. What is a Pollutant?
Abnormal presence or concentrations of a
constituent / substance or compound
Physical, chemical, biological…..
Inert or toxic
Indoor Air: Micro environment
Home & Work-place
Vehicles (cars, buses, trains, plains)
Crowded restaurants, clubs, bars
Theatres, shops, subways
3. Outdoor Air Pollution
Automobiles – Transportation exhausts
Industry – Gaseous and particulate
Fly ash
Liquid effluents etc.
Organic waste – Excreta
Vegetative matter
Material waste – Plastic pouches
Package material – wrappings
Quarries, Mines
Dust storms
5. Ambient Air Quality Standards
(Central Pollution Control Board)
Area Category SPM Permissible conc.
SO2 NOx CO
A Industrial &
mixed use
500 120 120 5000
B Residential /
Rural
200 80 80 2000
C Sensitive 100 30 30 1000
6. Deposition and clearance of Inhaled Particles
• Deposition: Sedimentation, Impaction,
Interception, Diffusion, Electro-static
precipitation
• Clearance: Muco-cilliary clearance, alveolar
macrophages, type I pneumocytes, lymphatics
or blood stream
• (4 kilos of dust may be inhaled in lifetime but
• only 10-80 g remain in lungs).
7. Harmful Effects of inhaled particles
• Biological factors e.g. allergens, pollens
• Chemical factors e.g. gases, quartz
• Physical factors: asbestos fibers
• Total Mass of dust inhaled is important
14. SILICOSIS
• Commonest, reported from all over the
country
• Pottery, ceramic, cutlery, slate, pencil,
metal casting, boiler scaling, grinding,
polishing, Glass, paints, rubber, sand
stone quarry, stone crushers
• Non occupational
15. Other Silicate Materials
• Nonfibrous
• Talc, Kaolin, Mica, Cement
• Fibrous
• Erionite (Fibrous aluminium silicate)
• Man made vitreous fibres e.g.
• Glass wool, rock wool, ceramic fibres
16. Asbestosis
• Asbestosis highly dangerous, but
extremely useful industrial material.
• Used in cement, building material, plastic,
insulation, fire proofing, ship building,
Railway workshops, cement & friction
product manufacture
• Environmental pollution is known.
17. OTHER DEPOSITION DISEASES
• Siderosis, Stannosis, Baritosis,
• Tungston, Carbon, Antimony
• Produce X-ray abnormalities, but no
functional change
• Minimal inflammatory response
18. ORGANIC DUST DISEASES
• OCCUPATIONAL ASTHMA
ALLERGIC ALVEOLITIS (HP)
• Agricultural exposures,
drug and chemical Industry
• Clinical picture
• Treatment
• Outcome
19. Byssinosis
• Cotton, Textile, Jute Industry
• 7-9% in Textile workers
• ‘Monday morning illness’, ‘Acute Mill
Fever’, ‘weavers’ cough
• Grades 0-3
• No long term effects
• Prevention: dust levels < 0.5 mg/m3
23. Indoor Air Pollution: Sources
1. Biomass Fuel Combustion
2. Environmental Tobacco Smoke (ETS)
3. Others:
Environmental – Air conditioning
Biological
Construction related – Paints, resins
Consumer products - Vapors
House dust (etc.)
Pet animals
4. Occupational
24. IAP Burden (Y 2000)
Global: 2.7% of global disease burden.
> 1.5 million deaths
India: 3.5% of national burden of disease
due to solid-fuel use.
> 0.4 million deaths
26. WHO Estimates on India (Y 2000)
1. Solid Fuel use 82% population
2. Deaths due to solid fuel use
ALRI (< 5 yrs) 251560
COPD (> 30 yrs) 155250
Lung cancer 340
Total: 407100
3. Total DALYs > 10 million
4. Percentage national burden
of disease 3.5
27. Effects attributed to short-term exposure
• Daily mortality
• Respiratory and cardiovascular hospital admissions
• Respiratory and cardiovascular emergency
department visits
• Respiratory and cardiovascular primary care visits
• Use of respiratory and cardiovascular medications
• Days of restricted activity
• Work absenteeism
• School absenteeism
• Acute symptoms (wheezing, coughing, phlegm, resp.
infections)
• Physiological changes (e.g. lung function)
28. Effects attributed to long term exposure
• Mortality due to cardiovascular and respiratory disease
• Chronic respiratory disease incidence and prevalence
(asthma, COPD, chronic pathological changes)
• Chronic changes in physiologic functions
• Lung cancer
• Chronic cardiovascular disease
• Intrauterine growth restriction (low birth weight at term,
intrauterine growth retardation, small for gestational age
Source: World Health Organization
29. Pyramid of health effects associated with air
pollution
Premature mortality
Hospital admissions
Emergency department visits
Visits to doctor Severity
of health
Restricted activity/reduced effect
performance
Medication use
Symptoms
Physiological changes in cardiovascular system
Impaired pulmonary function
Subclinical (subtle) effects
Proportion of population affected
Source: American Thoracic Society
34. Solid/Biomass Fuel Combustion
1. Increased BR in women exposed to BFC
(Jindal et al IJMR 1996)
2. Increased prevalence of respiratory symptoms in
women. 3608 of 3701 NS women: 13%
CB 1.9% (Highest in “chullah” users)
(Behera & Jindal, Chest 1991)
3. Higher prevalence of chronic bronchitis in rural
nonsmoker women (Jindal SK, IJMR 1993)
4. Poorer lung function in children (Behera et al 1998)
35. Environmental Tobacco Smoke (ETS)
Also called: Passive Smoking
Second-hand smoking
Side-stream smoking
Responsible for:
Respiratory problems
Heart and neurological problems
Cancers
Miscellaneous (Effects on Pregnancy
and children)
36. ETS Exposure and Respiratory Effects
1. Increased infections in children:
LRTI (Pneumonias and bronchitis)
Middle ear disease
(Internat Consultation Report on ETS 1999)
2. Detrimental effects on lung function and/or severity
of asthma in children
(Neuspiel et al 1989, Cohort study)
3. Increased asthma prevalence
Pooled OR (14 case control studies) = 1.37 (95% C.I. 1.15 – 1.64)
(Stracham & Cook 1998)
Pooled OR = 1.2 – 1.4 (Consultation Report 1999)
37. Pulmonary Effects of ETS (Indian Studies)
Children
1. Respir. Symptoms : (31%) OR = 1.6 to 2.25
(Gupta et al 2001)
• Ch./Recurrent cough in a sample of 2275
rural children at Ludhiana (Singh et al 2002)
2. Asthma Prevalence
• Chd.: Of 9090 students (9-20 yrs)
a greater no. of asthmatics had
smokers at home (41% vs 28%) OR = 1.78
(Gupta et al, 2001)
• ISAAC Questionnaire (Haryana) ETS risk OR = 3.33
38. ETS and Asthma in Adults
1. Increased morbidity in the previous one year period
• ER visits
• Hospitalization
• Requirement of parenteral bronchodilators, corticosteroids
and maintenance drugs
• Absence from work
(Jindal et al, Chest 1994)
2. Higher prevalence of ETS exposure in nonsmoker
patients with Acute Exacerbations (41% vs 20%)
(Jindal et al, Lung India 1997)
39. ETS and Lung Cancer
• Life time risk in NS who lived with a smoker = 24% (95%
C.I. 13% - 20%)
• Detection of tobacco specific carcinogens in blood of
ETS exposed NS
• Dose-response relationship of risk with cumulative ETS
exposure. (Review of 37 epidem. studies on 4626 cases)
(Hackshaw et al 1997)
Pooled RR (on meta-analysis of 43 of 76 studies and 20
meta-analysis reports) = 1.29 (95% C.I. 1.17 – 1.43)
(Taylor et al 2001)
40. ETS- Lung Cancer (Indian Studies)
1. Smoker: NS ratio (1:2.5 to 4)
(Jindal et al 1981, 1985; Behera et al 1992)
2. O.R. for ever smoking = 5.0(M), 2.47 (F)
(Gupta et al IJMR, 2001)
3. ETS exposure in lung Ca (case control)
• During childhood = OR = 3.9 (95% CI 1.9-8.2)
• Higher estimates for women; for cigarette
• A weaker association with smoking from
spouse; workplace and in vehicles
(Rapiti, Jindal, Gupta. Lung Cancer, 1999)
41. Prevention of IAP
1. Improvements in ventilation
2. Control of sources
3. Avoidance of indoor smoking and
combustion
4. Prevention of dampness
5. Adequate sunlight exposure
6. Proper disposal of body secretions
7. Care of the pet animals
42. Most of the health-hazards of
environmental pollution are man-made -
result from man’s assaults on
environment.
The best way of prevention therefore, is to
minimise the level and magnitude of these
assaults.
44. Lung responses to workplace hazards
DISEASE MECHANISM EXAMPLE
• Diffuse fibrosis Macrophage damage
Asbestos Type IV
hypersensitivit Beryllium
• Nodular Fibrosis Macrophage damage
Silica, Coal
• Emphysema Neutrophil enzymes Coal
• Bronchitis Mucosal Irritation Dust
• Asthma Chemotoxins
Cotton,
Wood, flour
• Allergic Alveolitis Cell mediated & Fungi
• Type II sensitivity
• Malignancy ? DNA damage
Asbestos,
Radon
45. Toxic biomass combustion pollutants and potential toxicity
Pollutant Known toxicological characteristics
Particulates (PM10, PM25) Bronchial irritation, inflammation, increased reactivity, reduced muco-
ciliary clearance, reduced macrophage response
Carbon monoxide Reduced oxygen delivery to tissue owing to formation of carboxy-
hemoglobin
Nitrogen dioxide (relative
small amounts from low
temperature combustion)
Bronchial reactivity, increased susceptibility to bacterial and viral lung
infections
Sulfur dioxide (relatively small
amounts from most bio-fuels)
Bronchial reactivity (other toxic end-points common to particulate
fractions)
Organic air pollutants
Formaldehyde
1,3 butadiene
Benzene
Acetaldehyde
Phenols, Benzo[a]pyrene
Dibenzopyrenes
Dibenzocarbazoles, cresols
Carcinogenicity
Co-carcinogenicity
Mucus coagulation, cilia toxicity
Increased allergic sensitization
Increased airway reactivity
Source: Bruce, Perez-Padila & Albalak; Cooper; Smith; Smith & Liu
46. Major health-damaging pollutants from indoor sources
Pollutant Major indoor sources
Fine particles Fuel/tobacco combustion, cleaning operations, cooking
Carbon monoxide Fuel / tobacco combustion
Polycyclic aromatic hydrocarbons Fuel / tobacco combustion, cooking
Nitrogen oxides Fuel combustion
Sulfur oxides Coal combustion
Arsenic and fluorine Coal combustion
Volatile & semi-volatile organic
compounds
Fuel / tobacco combustion, consumer products, furnishings, construction
materials, cooking
Aldehydes Furnishings, construction materials, cooking
Pesticides Consumer products, dust from outside
Asbestos Remodelling / demolition of construction materials
Lead Remodelling / demolition of painted surfaces
Biological pollutants Damp materials / furnishings, components of climate control systems,
occupants, outdoor air, pets
Radon Soil under buildings, construction materials
Free radicals and other short-lived,
highly reactive compounds
Indoor chemistry
Source: Zhang & Smith
47. HISTORY
• Prehistoric : Mining fit for convicts and slaves
• (1556) Georgius Agricola: dangers of
suffocation
• (1713) Ramazzini: Breathlessness in grain
handlers – Father of occupational medicine
• (1879) Lung cancer in metal miners
• ‘Asbestos’ related diseases
• 1930 – fibrosis
• 1949 - Carcinoma
• 1960 – Mesothelioma
51. 3. Increased BR in ETS exposed nonsmoker
women with asthma
(Jindal et al IJCDAS 1999)
4. Increased BR in nonsmoking asymptomatic
ETS exposed women
(Jindal et al IJMR 1996)