저층 침적 위험·유해물질(Hazardous and Noxious Substances)은 해저에 침적되는 위험·유해물질로 직접 및 광학 탐지 기법의 적용 이 어렵기 때문에 수중에서 효과적인 음향 탐지 기법 적용이 요구된다. 본 연구에서는 저층 침적 위험·유해물질인 클로로폼(Chloroform)을 이용한 후방산란신호 측정 실험을 통해 저층 침적 위험·유해물질 음향 탐지 가능성을 확인하였다. 제작된 아크릴 수조 내에 지점토를 이 용하여 웅덩이를 만든 후 Pan&Tilt를 이용하여 수평입사각을 90°에서 50°까지 0.5° 간격으로 변화시켜가며 클로로폼 유무에 따른 후방산란 신호 측정이 수행되었다. 송수신기를 단상태로 주파수 200 kHz, 신호길이 25 인 정현파 신호를 이용하여 송수신하였으며, 클로로폼 유 무에 따른 후방산란신호를 측정하였다. 클로로폼이 침적된 경우 수평입사각 약 80°이하에서 물과 클로로폼 경계면에서의 후방산란신호 수신준위가 작아지는 것이 확인되었다. 물과 클로로폼 경계면에서의 후방산란신호 측정된 결과를 통해 저층 침적 위험·유해물질 음향 탐 지 가능성을 확인하였다.

Chronic inflammation, which results from continuous exposure to antigens, is one of major reasons for tissue damage and diseases such as rheumatoid arthritis and type 2 diabetes. In this study, we investigated the anti-inflammatory effects of extracts (hexane, CHCl3, MeOH, MeOH/H2O, and H2O) from GW10-45, which is our new cultivar of an edible mushroom Pleurotus ferulae (ASI 2803 and ASI 2778), in RAW264.7 murine macrophages. None of the extracts showed cytotoxicity in RAW264.7 cells and the hexane, CHCl and H extracts reduced nitric oxide (NO) production, an important inflammatory marker, in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. Particularly, the extract (CG45) inhibited NO production more than the other extracts did. To elucidate the effects of CG45 on molecular targets involved in proinflammatory responses, we performed western blot analysis. Expression of inducible nitric oxide (iNOS) significantly decreased in LPS and CG45 co-incubated cells compared to that in LPS only-treated cells. Additionally, another protein thatplays a critical role in inflammation, was down-regulated in cells treated with both LPS and CG45. In the nuclear factor (NF)- B pathway, phosphorylation of I Bα decreased in RAW264.7 cells treated with both LPS and CG45. Furthermore, CG45 inhibited the phosphorylation of NF- B in LPS-stimulated RAW264.7 cells. Conclusively, CG45 could suppress proinflammatory responses in LPS-stimulated RAW264.7 cells by down-regulating not only the phosphorylation of NF- B and I Bα but also the expression of iNOS and COX-2 without any cytotoxicity.

Recently, bathes have been suspected to an important source of indoor exposure to volatile organic compounds(VOCs). Two experiments were conducted to evaluate chloroform exposure and corresponding body burden by exposure routes while bathing. Another experiment was conducted to examine the chloroform dose during dermal exposure and the chloroform decay in breath after dermal exposure. The chloroform dose was determined based on exhaled breath analysis. The exhaled breath concentration measured after normal baths (2.8 ㎍/㎥) was approximately 13 times higher that measured prior to normal bathes (0.2 ㎍/㎥). Based on the means of the normalized post exposure chloroform breath concentration, the dermal exposure was estimated to contribute to 74% of total chloroform body burden while bathing. The internal dose from bathing (inhalation plus dermal) was comparable to the dose estimated from daily water ingestion. The risk associated with a weekly, 30-min bath was estimated to be 1 x 10^-5, while the risk from daily ingestion of tap water was to be 0.5 × 10^-5 for 0.15 1 and 6.5 × 10^-5 for 2.0 1. Chloroform breath concentration increased gradually during the 60 minute dermal exposure. The breath decay after the dermal exposure showed two-phase mechanism, with early rapid decay and the second slow decay. The mathematical model was developed to describe the relationship between water and air chloroform concentrations, with R^2 = 0.4 and p<0.02.

The pyrolysis reactions of atomic hydrogen with chloroform were studied in a 4 cm i.d, tubular flow reactor with low flow velocity (518 ㎝/sec) and a 2.6 ㎝ i.d. tubular flow reactor with high flow velocity (1227 ㎝/sec). The hydrogen atom concentration was measured by chemiluminescence titration with nitrogen dioxide, and the chloroform concentrations were determined using a gas chromatography. The chloroform conversion efficiency depended on both the chloroform flow rate and linear flow velocity, but did not depend on the flow rate of hydrogen atom. A computer model was employed to estimate a rate constant for the initial reaction of atomic hydrogen with chloroform. The model consisted of a scheme for chloroform-hydrogen atom reaction, Runge-Kutta 4th-order method for integration of first-order differential equations describing the time dependence of the concentrations of various chemical species, and Rosenbrock method for optimization to match model and experimental results. The scheme for chloroform-hydrogen atom reaction included 22 elementary reactions. The rate constant estimated using the data obtained from the 2.6 cm i.d. reactor was to be 8.1 × 10 exp (-14) ㎤/molecule-sec and 3.8 × 10 exp (-15) ㎤/molecule-sec, and the deviations of computer model from experimental results were 9% and 12%, for the each reaction time of 0.028 sec and 0.072 sec, respectively.

The use of chlorinated water in swimming pools produces elevated chloroform levels in the water and air of the pools which can cause chloroform body burden of swimming individuals. Present study confirmed the chloroform body burdens from a 40-min swimming and evaluated the decay of chloroform breath concentration after the cessation of a 60-min swimming. Air and water concentrations were measured in the pools. The water and air chloroform concentrations ranged from 18.1 to 25.3 ㎍/ℓ and from 30.9 to 60.7 ㎍/㎥ for the confirmation study, respectively. The breath level after 40-min swimming was about 64 to 266 folds higher than the corresponding background breath. The breath concentration after the 40-min swimming ranged from 10.5 to 21.3 ㎍/㎥, while that prior to the corresponding swimming ranged from 0.07 to 0.19 ㎍/㎥. In addition, the post-exposure breath level varied with the subjects who swam in the pool on the same visiting day. Breath concentration increased gradually during 60-min swimming, then decreased rapidly within 5 minutes after the cessation of exposure, after that, decreased slowly, and finally approached to a background breath level at 1-2 hr after exposure.

There has been an increased awareness of the need to confirm the chloroform exposure associated with using chlorinated household water. Ten of a 30-minute tub bath were normally taken by two volunteers in a bathroom of an apartment. Chloroform concentrations were measured in bathing water and bathroom air, and exhaled breath of the subjects prior to and after bathing. Bathing using chlorinated tap water resulted in a chloroform exposure and caused a body burden. Based on the difference of chloroform concentrations between breath samples collected prior to and after bathing, the chloroform body burden from a 30-minute bath was estimated to be about 8 to 26 folds higher than that prior to the bath. The mean water and bathroom air chloroform concentrations measured to evaluate the body burden were 9.4 ㎍/ℓ and 14.9 ㎍/㎥, respectively. The chloroform level of the bathroom air was 34 to 130 times higher than that of the living-room air. The relationship between the bathroom air and the corresponding breath chloroform concentrations were significant with p=0.03 and R^2=0.47.

Chloroform present in the swimming water disinfected with sodium hypochlorite is released to the air of swimming pools. The air chloroform concentrations were measured in two swimming pools A and B which applied both sodium hypochlorite and ozone. Their mean concentrations are 28.0 ㎎/㎥ and 33.6 ㎍/㎥ in the swimming pools A and B, respectively. On the other hand, the mean water chloroform concentrations in the swimming pools A and B were 23.9 ㎍/ℓ and 19.5 ㎍/ℓ, respectively. The air chloroform concentrations were lower in the swimming pools A and B than those reported by previous studies abroad employed the swimming pools which applied sodium hypochlorte only for water disinfection. The water chloroform concentrations were also lower in this study than in the previous studies. The relationship between the air and water chloroform concentrations measured in this study was significant with p=0.002 and R^2=O.42. At similar time to the indoor air sampling, outdoor air samples were collected at two sites near each of the swimming pools A and B. The mean outdoor air chloroform concentrations near the swimming pools A and B were 0.41 ㎍/㎥ and 0.16 ㎍/㎥, respectively. The outdoor air chloroform concentrations measured in this study were equal to or lower than those reported by previous studies abroad. The chloroform dose inhaled for a typical one-hour swim was estimated to be 25.9 ㎍ per person, corresponding to a specific 0.37 ㎍/㎏ body weight. for a reference 70 ㎏ male adult, while the inh lation dose of chloroform from the outdoor air was estimated to be 5.6 ㎍ per person per day, corresponding to a specific 0.08 ㎍/㎏/day for the same reference male adult.

Chlorinated water in swimming pools contains chloroform at elevated levels compared to chlorinated drinking water. Chloroform levels in four indoor swimming pools(swimming pools A, B and C in a city of Korea and swimming pool D in a city of New Jersey in the United States) were examined. The chloroform levels in the water of swimming pool C (city-managed) were shown to be significantly(p=0.0001) different from those of private swimming pools A and B: the mean chloroform levels in the pools A, B, and C are 22.8, 17.8, and 31.1 ㎍/ℓ respectively. Furthermore, all of these chloroform levels are significantly(p=0.0001) different from those of New Jersey: chloroform concentration of the Korean pools ranged from 10.9 ㎍/ℓ to 47.9 ㎍/ℓ with a mean of 23.2 ㎍/ℓ, while it ranged from 27 ㎍/ℓ to 96 ㎍/ℓ with a mean of 64.4 ㎍/ℓ in the New Jersey pool. The disinfection processes would cause part of this difference since the swimming pools in Korea applied both chlorination and ozonation method, while the swimming pool in New Jersey used chlorination method only. It was implied that swimming parameters inconsistently vary, resulting in fluctuation of and no constant accumulation of chloroform in the water with the change of time for the day. A regression analysis showed no relationships between sampling time and chloroform concentrations for the sampling day in the swimming pools of Korea. A F-test indicated no significant difference of chloroform concentrations in the morning and afternoon samples collected in the swimming pools. Ingestion dose was estimated to be 0.58 ㎍ from an hour swimming in a city of Korea, taking into accounting an average of 23.2 ㎍/ℓ in swimming pools in the city. In extreme situation, the ingestion dose was estimated to he 12.0 ㎍ from an hour swimming in a city of Korea.