Selamat Datang Ke Portal Rasmi Kementerian Kesihatan Malaysia

DataTerbuka

Broadcast
Pengenalan Kami
Berita
Soalan Lazim
Publication
Pekeliling
OpenData
Hubungi Kami
 
 
     FAQSoalan Lazimhubungikami Hubungi Kamiaduan Aduan & Maklum Balaspetalaman Peta Laman
     
Bahasa Melayu | English | Lain-Lain Bahasa  
header_new__logo

Advisory Note For Smokers To Stop Smoking During Haze

Advisory Note For Smokers To Stop Smoking During Haze

 

 

Introduction

Haze is traditionally an atmospheric phenomenon where dust, smoke and other dry particles obscure the clarity of the sky. The World Meteorological Organization manual of codes includes a classification of horizontal obscuration into categories of fogice fogsteam fogmist, haze, smokevolcanic ashdustsand and snow. Sources for haze particles include farming (ploughing in dry weather), traffic, industry, and wildfires.

 

Haze often occurs when dust and smoke particles accumulate in relatively dry air. When weather conditions block the dispersal of smoke and other pollutants they concentrate and form a usually low-hanging shroud that impairs visibilityand may become a respiratory health threat. Industrial pollution can result in dense haze, which is also known assmog.

 

For these reasons, sunrise and sunset colors appear subdued on hazy days, and stars may be obscured at night. In some cases, attenuation by haze is so great that, toward sunset, the sun disappears altogether before reaching the horizon.

 

The main pollutant of concern to health during a smoke haze is the fine particulate matter or PM10 (particulate size of 10 micron and below). The health effect depends on the severity of the smoke haze as described by the PSI (Pollutant Standards Index) reading. At PSI > 100, the air quality is deemed UNHEALTHY.

 

The air quality in Malaysia is reported as the API or Air Pollutant Index. Four of the index's pollutant components (i.e., carbon monoxide, ozone, nitrogen dioxide and sulfur dioxide) are reported in ppmv but PM10 particulate matter is reported in μg/m3.

 

Pathophysiology of smoking and respiratory defence mechanism

The innate defense system of the lung includes the apparatus for producing and clearing mucous, the epithelial cell barrier and infiltrating inflammatory immune cells.

 

Chronic stimulation of this system by the tobacco-smoking habit results in both increased production and decreased clearance of mucous from the airway’s lumen, causing disruption of the tight junctions that form the epithelial barrier and infiltration of the damaged tissue by polymorphonuclear and mononuclear phagocytes as well as natural killer cells and CD4+ and CD8+ T cells and B-cell lymphocytes. The adaptive immune response requires antigen presentation primarily by dendritic cells and the organization of the lymphocytes into follicles with germinal centres.

 

This type of response is rarely found in healthy non-smokers but has been documented in about 5 percent of peripheral lung units of smokers with normal lung function, increasing to about 20 to 30 percent of airways in the later stages of chronic obstructive pulmonary disease.

 

Resultant effect of both smokers and haze

The persistent innate and adaptive immune inflammatory response present in the lungs of all long-term smokers appears to be amplified in those smokers who develop severe COPD. Cigarette smoke when inhaled directly or second-hand smoke exposure comprising more than 7,000 chemicals; whereby hundreds of these are hazardous and at least 69 are known to cause cancer, provides an extraordinary strong dose of free radicals to the lung coupled with an exacerbation of a synergistic effect due to the particulate pollutant components (i.e., carbon monoxide, ozone, nitrogen dioxide and sulfur dioxide) from the haze which is rapidly absorbed by cells in the body and produce disease causing cellular changes. This also initiates processes of oxidative injury that involve multiple cell types and the entire lung.

 

Local inflammation results and markers of inflammation becomes higher, both in smokers and in persons with COPD, than are those in non-smokers. Oxidative stress unfavourably tips the protease-antiprotease balance toward protease, leading to tissue damage and COPD.

 

The tobacco smoke, which comprises an aerosol (a mixture of solid and liquid particles) and gases, has thousands of chemical components, including many well-characterized toxins and carcinogens (International Agency for Research on Cancer [IARC] 2004). Many of these components are in the gaseous phase and others are components of the particles coupled with the particulate pollutant components (i.e., carbon monoxide, ozone, nitrogen dioxide and sulfur dioxide) from the haze. With this involuntary inhalation resultant effect have the potential to injure the airways and alveoli.

 

The size of particles in the smoke inhaled directly from a cigarette (mainstream smoke) has been studied and indicates that the mass median aerodynamic diameter of particles is 0.3 to 0.4 micrometers (μm) (Martonen 1992; Bernstein 2004). Particles of this size penetrate to and are deposited in the deep lung. This is eventually coupled with the inhalation of particulate pollutant components which measures the particulate size of 10 micron and below) in the smoky haze.

 

This resultant effect of exposure both to cigarette smoke and the inhalation of particulate pollutant components from the haze would result in an obstructive ventilatory defect with a decreased FEV1 / FVC; restrictive ventilatory defect resulting in a decreased TLC; abnormal uptake of gas by Hgb across alveolar capillary membrane and disorders with airway dysequilibration (emphysema). The substantial volume of air inhaled daily by an adult which amounts to 10,000 litres per day together with the harmful impurities (arising both from cigarette smoke and haze) results in deterioration of the pulmonary function capabilities of an individual.

 

A causal conclusion on smoking and deterioration of pulmonary function capabilities with exposure to haze

This infers a causal conclusion of a deterioratory effect  between smoking and all major respiratory symptoms among adults, including coughing, phlegm, wheezing, dyspnoea, breathlessness among children of school age, poor asthma control amongst adults and children of school age, and chronic obstructive pulmonary disease, for both active smoking and involuntary exposure to tobacco smoke during haze.

 

A Serious Notation From The Ministry of Health Malaysia

Stop smoking immediately in haze environments in order to sustain your pulmonary function capabilities healthily. 


  •  
  • Print
  • Email this page