The patient in our case was a 66-year-old man.
His chief complaint was the abnormality observed in his chest computed tomography (CT) images.
The patient was initially suspected of having an ulcerative invasive tumor in his stomach based on endoscopic findings by a clinic in Pusan on September 8, 2012. He then underwent total gastrectomy for gastric cancer at Pusan National University Yangsan Hospital on October 2, 2012, followed by six cycles of chemotherapy between January 27, and May 28, 2013. After a chest CT scan on November 11, 2013, he was diagnosed with asbestosis and transferred to the Department of OEM for further evaluation of the association between asbestosis and gastric cancer in his case.
The patient in this case had a history of hypertension. He reported smoking 23-packs-per-year until 1995 and consuming one bottle of Soju (alcohol) per week prior to his gastric cancer surgery.
The patient worked in a textile factory with no asbestos exposure for 18 years (from 1966 to 1983). He later performed asbestos spinning and weaving work for 11 years (from 1983 to 1993) using chrysotile at Masan Gwangsum (1983 - 1984), Seongjin Chemical (1985 - 1992), and in Taehwa Capaxeal (1993).
His asbestos-spinning job involved mixing chrysotile with synthetic fiber during a 12-hour shift (from 8 a.m. to 8 p.m.).The job site was full of white dust, and despite wearing a mask, he still found dust around his nose when finishing work. Between 1987 and1990, as a plant manager, he managed the entire process that involved mixing asbestos and synthetic fiber, spinning, twisting, and weaving. Additionally, he directly spun asbestos.
The patient looked healthy at presentation. His blood pressure was 130/70 mmHg; body temperature was 36.6 C; pulse rate was 80 beats/minute, and respiratory rate was 20 times/minute. His conjunctiva was not anemic, and anicteric sclera was observed. His chest auscultation revealed fine crackles of end inspiration in the lower areas of both lungs. His heartbeat was regular, and no heart murmur was detected. The physical examinations showed no abnormal findings in his abdomen or skin, and no club fingers or cyanosis in his extremities.
In a pulmonary function test conducted on November 18, 2013, the patient's forced expiratory volume at timed intervals of a second (FEV1) was 2.24 L (72% of the expected value); his forced volume vital capacity (FVC) was 2.52 L (61% of the expected value), and his FEV1/FVC was 89% of the expected value, which showed a mildly restrictive ventilator disturbance. His pulmonary diffusion capacity of carbon monoxide (DLco) was within the normal range at 15.9 ml/min/mmHg (77% of the expected value).
The chest CT images obtained on November 11, 2013 showed typical asbestosis findings of pleural thickening and calcification in both thoracopulmonary cavities, subpleural fine reticular opacity in the lungs, ground glass opacity, and honeycomb appearance (Figure 1). There were no significant findings from the chest X-ray images.
In the upper gastrointestinal (GI) tract endoscopy conducted at a clinic in Pusan on July 3, 2010, reflux esophagitis and erosive gastritis were observed. Another upper GI tract endoscopy conducted on September 8, 2012 showed campylobacter-like organisms (CLOs) (+), suspected progressive gastric cancer, and atrophic gastritis (Figure 2).
The post-operative pathologic examination conducted on October 4, 2012 confirmed that the mass measuring 4.9 x 4.5 cm and located in the anterior wall of the stomach body was an adenocarcinoma (Figure 3).
According to studies on asbestos levels in factories handling the chemical, the mean value before 1990 was 4.3 f/cc (standard deviation[SD] 4.3 f/cc), and that in 1990 was 2.3 f/cc (SD = 1.7 f/cc). The cumulated exposure of the patient in this case was calculated as follows:
Thus, his level of cumulated exposure in the patient was estimated to be 38.0-71.0 f-yr/cc. According to the Helsinki criteria for asbestos-related diseases, the relative risk of developing lung cancer more than doubles when the cumulated exposure to asbestos is 25 f-yr/cc or higher.
Considering the patient's work experience with chrysotile in the textile factory and his past working environment, he was thought to have been exposed to high level of asbestos.
Asbestos fiber exposure is reportedly associated with gastric cancer. In this case, the patient worked for 11 years weaving and spinning asbestos. Therefore, the possibility of gastric cancer caused by asbestos fiber exposure could not be completely excluded. In the meta-analysis of the association between asbestos fiber exposure and gastric cancer that compared any exposure versus none, the summary relative risk was calculated to be 1.17 (95% confidence interval [CI], 1.07-1.28). Similarly, in the comparison of high-dose asbestos fiber exposure versus no exposure, the summary relative risk was calculated to be 1.31-1.33.
The standard mortality rate (SMR) of gastric cancer tends to increase when that of lung cancer does. Since the cumulative asbestos fiber exposure of this patient was 38.0-71.0 f-yr/cc, and his relative risk of developing lung cancer was more than two times, the SMR of gastric cancer was 1.34 (95% CI, 1.07-1.67) when that of lung cancer was > 2.00. When the SMR of lung cancer was >3.00, that of gastric cancer was 1.43 times higher.
The risk of asbestos fiber exposure was determined based on the incidence of lung cancer caused by such exposure and information obtained from the exposure evaluation. According to the United States Environmental Protection Agency (US EPA), there are three routes of asbestos fiber exposure: ingestion, respiration, and skin exposure. However, asbestos is rarely absorbed through the skin, and no carcinogenic risk from ingestion has been reported. Therefore, the ELCR from respiration was calculated to evaluate the health risk from asbestos exposure using the following equation.
EPC was calculated as 4.3 f/cc x 24/8 h using the reported asbestos concentration in factories handling the chemical. Time weighted average in this case was calculated using asbestos fiber exposure time, considering that the patient worked for 12 hours per day and 5 days per week (12/24 h/day x 260/365 days/yr). During his 11 years of exposure, the IUR was 2.1 x 10-2.
The theoretically acceptable carcinogen risk that corresponds to the natural death rate is 1.0 x 10-6 (one out of one million). However, in cases of environmental carcinogens, the acceptable risk is practically one in 100,000, considering the profit/loss against investments and status of engineering and analytical technologies. The World Health Organization also suggests that the ELCR of carcinogenic substances is 1.0 x 10-5 (one out of 100,000). The ELCR of lung cancer for this patient was 9,648 x 10-5, which translated to an excess cancer risk of 9,648 in 100,000.