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We performed congener specific analysis of dioxins using HRGC/HRMS and determined their lipid based concentrations in blood samples collected from 175 family members living with certificated Yusho patients and considered as Yusho patients (Family members living with Yusho patients) during annual Yusho examinations between 2013 and 2021. When concentration of 2,3,4,7,8-pentachlorodibenzofuran (PeCDF) was compared in eleven Family members living with Yusho patients, undergoing examinations among the nine years, the longitudinal concentrations in the respective individuals hardly changed over these years. Mean concentration of 2,3,4,7,8-PeCDF in blood from 175 Family members living with Yusho patients was calculated as 25 pg/g-fat, which was higher than the mean value of 12 pg/g-fat in blood from 409 Yusho-suspected (non-registered) persons. The rates of persons with blood 2,3,4,7,8-PeCDF concentrations below 50 pg/g-fat in the entire Family members livingwith Yusho patients occupied approx. 90 %, on the other hand, concentrations above 50 pg/g-fat, defined as high concentration in Yusho criteria, were also found in fourteen Family members living with Yusho patients.

In 1968, more than 2,000 peoples were exposed to high concentrations of dioxin-like compounds by eating rice bran oil contaminated with 2,3,4,7,8-pentachlorodibenzofuran (2,3,4,7,8-PeCDF), polychlorinated biphenyls, and polychlorinated quarter phenyls. These Yusho (oil disease in Japanese) patients have been suffered from various symptoms such as general malaise, chloracne, hyperpigmentation, sputum and cough, hyperesthesia or numbness of extremities since then. The blood concentrations of 2,3,4,7,8-PeCDF, major causal agent for toxicity, are still very high in many Yusho patients even now. Dioxins exert their major toxicity by binding and activating arylhydrocarbon receptor (AHR) and subsequent generation of reactive oxygen species (ROS). In addition, recent studies have revealed a pathogenic role of AHR in manifestation of various Yusho symptoms. Moreover, medicinal agents which inhibit AHR activation and ROS production (antioxidative AHR inhibitor) may be applicable for the treatment of Yusho patients. In this review, we summarize current topics on Yusho and its therapeutic approach with special reference to AHR.

Our previous studies have revealed that maternal exposure to2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) attenuates the hypothalamic biosynthesis of gonadotropin-releasing hormone (GnRH) in male offspring, thereby imprinting sexual immaturity. To clarify the mechanisms underlying such reductions in GnRH, we examined the effects of TCDD on the number and/or form of GnRH neurons. Maternal exposure to TCDD was found to have little effect on the number or location of GnRH neurons in male offspring at gestational day 20 (GD20), postnatal day 4 (PND4), PND7, PND14, or PND28. However, maternal exposure to TCDD was observed to attenuate the number of bipolar GnRH neurons in the male offspring at PND14 and PND28, although no similar effect was observed for unipolar neurons. Furthermore, we detected no obvious effect of TCDD on the axonal length of GnRH neurons. These findings indicate that TCDD reduces the number of bipolar GnRH neurons beginning at PND14 when it causes GnRH attenuation. TCDD may thus elicit the attenuation of GnRH neurons in a bipolar neuron-selective manner.

Yusho, occurred in 1968, is an intoxication of high concentrations of polychlorinated dibenzofurans and their related compounds. Like other intoxication by dioxin-like compounds, one of the major symptoms of Yusho is skin symptom such as chloracne and pigmentation. Dioxins exert their major toxicity by binding and activating aryl hydrocarbon receptor (AHR) and subsequent generation of reactive oxygen species (ROS). Sustained and exaggerated AHR activation by dioxins accelerates the keratinization of keratinocytes and converts the sebaceous differentiation of sebocytes to keratinocyte-like differentiation which results in loss of sebocytes and cyst formation of hair follicle, leading to chloracne. AHR activation by dioxins upregulates the melanogenesis of melanocytes, leading to pigmentation. Phytochemical Kampo drugs which inhibit AHR activation and subsequent ROS production are potential treatment for Yusho patients.

Maternal exposure to dioxin produces a number of developmental toxicity, such as growth retardation and defects in sexual dimorphic behaviors in offspring. Our previous studies have found that the toxic effects induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a highly toxic congener of dioxins, are due to a reduction in the pituitary expression of growth hormone (GH) and luteinizing hormone (LH) during the fetal period, via activation of the aryl hydrocarbon receptor (AHR). In this study, we examined whether 2,3,7,8-tetrafluorodibenzo-p-dioxin (TFDD), the analog of TCDD in which chlorine atoms are replaced with fluorine atoms, can antagonize dioxin toxicity. In T47D cells, TCDD (0.5 nM) dramatically increased the activity and expression of cytochrome P450 1A1 (CYP1A1), a representative gene induced by AHR activation. However, TFDD co-treatment suppressed the induction in a dose-dependent manner. Its median effective dose (ED50) was estimated as 45.9 nM. In contrast, although exposing 1 mg/kg TCDD to pregnant rats attenuated the expression of LHb and GH mRNA and induced the expression of CYP1A1 mRNA in the male fetal pituitary, daily oral administration of TFDD (1 mg/kg/day) to the TCDD-exposed dams did not have any suppressive effects. These results suggest that maternal treatment with TFDD, even at 1,000 times the dose of TCDD, cannot block dioxin-produced developmental toxicity in fetuses.

Yusho, the mass food poisoning, occurred in western Japan in 1968. PCBs and dioxin like compounds such as 2,3,4,7,8-PeCDF were detected as causal chemicals for Yusho. Our group have measured blood concentrations of dioxin-like compounds and analyzed their half-lives. In our previous studies, we have found two groups ; one group has 7-10 years of half-lives as reported by other researchers, and the other group has near infinite half-lives. In addition, the number of patients in group showing 7-10 years of half-lives decreased and the number in group with near infinite half-lives increased. However, those changes were not evaluated in individual patient since follow-up period was relatively short to analyze the individual half-live. Therefore, we now intend to evaluate the long-term change of half-life in individual patient. Our preliminary analysis indicates that the half-life of 2,3,4,7,8-PeCDF appears to be prolonged in each patient. Considering the recent low levels of environmental contamination of dioxins and their related compounds, the prolonged half-life of blood concentration of 2,3,4,7,8-PeCDF points its deteriorated excretion.

Background : Our previous pilot study suggested high rates of insomnia among 140 patients with Yusho, a condition caused by exposure to dioxins and dioxin-like compounds. Moreover, higher blood concentrations of dioxin were associated with lower subjective sleep quality. / Objectives : In this cross-sectional study, we analyze data from a Japanese nationwide survey that was designed to investigate the relationship between insomnia and dioxin toxicity among patients with Yusho. / Methods : For this study, 899 participants (46.3% men, median age [IQR] : 66 [58-78] years) were recruited. Symptoms related to insomnia were assessed. Toxicity of dioxins and dioxin-like compounds was evaluated with the total toxic equivalent quantity (TEQ), which is the summation of each TEQ calculated from the blood concentrations of 21 congeners of dioxin and dioxin-like compounds. Logistic regression analysis for insomnia were adjusted by age, sex, body mass index, habitual drinking, and smoking status. / Results : The number of participants with difficulty initiating and/or maintaining sleep (DIMS) was 753 (53.4％). Total TEQ was categorized on the following quartiles : first quartile (Q1)＜20 (reference, second quartile (Q2) = 20-35, third quartile (Q3) =35-62, and fourth quartile (Q4)≧62 pg-TEQ/g lipid). Adjusted odds ratios (95% confidence interval) for DIMS of Q2-4 were 1.89 (1.23-2.89), 1.62 (1.02-2.57), and 2.09 (1.24-3.53), respectively. / Conclusions : Insomnia was frequent among patients with Yusho. Insomnia was associated with not only the apparently high level of total TEQ, but also the level of total TEQ observed among general population. In the pathophysiology of insomnia, dioxins and dioxin-like compounds, which persist in environment and human body for a long time, might be one of the environmental factors among patients with Yusho and general population.

We performed congener specific analysis of dioxins using HRGC/HRMS and determined their concentrations in blood samples collected from approx. 1,700 persons during annual Yusho examinations between 2001 and 2017. When concentration of 2,3,4,7,8-pentachlorodibenzofuran (PeCDF) was compared in seven Yusho patients undergoing examinations among the seventeen years, the longitudinal concentrations in the respective individuals hardly changed over these years. Mean concentration of 2,3,4,7,8-PeCDF in blood from Yusho patients registered by annual inspections for Yusho was calculated as 110 pg/g, which was 80％ higher than the mean value of 17 pg/g in normal controls, and the rates of persons with blood 2,3,4,7,8-PeCDF concentrations below 50 pg/g in the entire patients occupied approx. 60％. On the other hand, in a subset of Yusho patients registered by the supplemental criteria revised on 2012, it was found that the median values of concentration of 2,3,4,7,8-PeCDF were similar to the those of normal controls.

Hepatic expression of selenium binding protein (SelenBP) in female mice and its inducibility by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) was studied using wild-type (WT) C57BL/6J and SelenBP1-knockout mice. Female WT mice (4 weeks old) received TCDD at the dose of 100 mg/kg (i.p.). The control group received the vehicle, corn oil. In addition, SelenBP1-KO mice received TCDD at the same dose as the WT. A control group of SelenBP1-KO mice received the vehicle, corn oil. Five days after treatment, livers were removed and homogenized. The level of SelenBP in the liver homogenate was compared between the control and TCDD-treated groups by immunoblotting using anti-human SelenBP1 antibody as the primary antibody. It has been discovered that there are two SelenBP isoforms in mice, SelenBP1 and SelenBP2. The antibody used was expected to recognize both SelenBP1 and SelenBP2 in mice. The level of SelenBP in the livers of female SelenBP1-KO mice was far lower than those in WT mice. In addition, the level of SelenBP in WT mice was induced to approximately 5 times by TCDD treatment while there was no substantial increase in SelenBP level in SelenBP1-KO mice. Therefore, SelenBP1 is constitutively expressed as the predominant SelenBP isoform in the liver of female WT mice whereas the level of SelenBP2 remains low. In addition, the SelenBP2 is barely induced in the liver of female mice by TCDD. These results suggest that the induction of hepatic SelenBP at the protein level in female mice by TCDD is mainly due to the induction of SelenBP1.

We developed solvent-cut large-volume injection system (SCLV) using Deans switch type SilFlow in dioxins measurement of human blood. The SilFlow worked in the same mechanism as the conventional SCLV for dioxins measurement, showed high reproducibility in dioxins measurement of the standard solution and the control sample. Since the SilFlow has very small dead volume as compared with the conventional method, the influence of contamination is small, and the handling is easy. In this study, we proved that SilFlow is available for an alternative to SCLV in blood dioxins analysis.

Maternal exposure to dioxins causes a number of developmental disorders in the offspring. Previous studies have suggested that lactational exposure to 2,3,7,8-tetrachlorodizenzo-p-dioxin (TCDD) reduces the pup level of thyroid hormone after weaning, leading to the damage to their development including neural maturation. However, the specificity for age and dioxin congeners as well as dose dependency in terms of a reduction in pup thyroid hormone remains to be clarified. To address this issue, we investigated whether TCDD or 2,3,4,7,8-pentachlorodibenzofuran (PenCDF), one of the dioxins which caused 'Yusho' incident, affects the status of thyroid hormone during the fetal and neonatal periods. Treating pregnant rats at gestational day (GD)15 with 1 μg/kg TCDD scarcely affected the serum concentration of thyroxine, although a significant reduction by TCDD was detected at limited endpoints [GD21 and postnatal day (PND)21]. In addition, maternal exposure to TCDD (0.05-30 μg/kg) or PenCDF (1-1,000 μg/kg) did not have any change in the serum level of thyroxine in GD20 fetuses even at the maximum dose. Neither the expression of pituitary thyroid-stimulating hormone β (TSHβ) nor hypothalamic thyrotropin-releasing hormone was sensitive to TCDD treatment. In pregnant dams, TCDD decreased the serum level of thyroxine at GD20 and 21, while the pituitary expression of TSHβ was induced. These results suggest that a single administration of dioxins to pregnant rats at GD15 have little effect on the level of thyroxine in the fetuses and infants, while a reduced level of this hormone observed in the offspring at GD21 and PND21 and pregnant dams at GD20 and 21.

We developed an analytical method for accurately determining the concentrations of dioxin and polychlorinated biphenyls(PCBs) in a blood volume of 5 g. Inter-laboratory crosscheck is available for maintaining the quality of dioxin and PCB analysis. We carried out the crosschecks of dioxin and PCB analysis in the blood with domestic analysis organizations. Two crosschecks each of dioxin and PCB analysis were carried out from 2007 through 2011. As a result, the findings of our analysis accorded well with the analyses of the other organizations. We believe that our analytical method is sufficiently reliable.

実験動物に対するダイオキシンの胎盤・母乳経由暴露により若年期において行動異常が発現することが知られている。しかし,異常行動の正確な発現時期(発症時期)および性差は明らかになっていない。我々は,ダイオキシン周産期暴露に起因する行動異常発症は性ホルモン分泌調節と関連性があると推察し,それを示す論拠を得るために本研究を行った。正常な雌雄のddY系マウスを交配して妊娠させ,妊娠7日日と14日目にオリーブオイルに溶解した2,3,7,8 tetrachlorodibenzo-p-dioxin (TCDD)を100 μg/kg,またはオリーブオイルを経口投与した。産仔をそれぞれの母マウスに母乳飼育させ,生後28日に離乳した。その後,同腹の同性産仔同士で集団飼育し,生後12週まで日視による行動観察および接触刺激応答計測装置を用いた行動学的定量調査を行った。TCDDを胎盤・母乳経由で摂取した産仔の多くには,弱い接触刺激または視覚刺激に対して過敏に応答する行動,すなわち接触逃避行動および対物攻撃行動が顕著に発現した。両行動の発現時期を特定する目的で,接触刺激応答計測装置を用いて生後5週から生後12週に至るまで,週3日,両行動の強度を定量的および力学的に計測した。その結果,両行動は,雄産仔において生後7週末から8週に有意に増大し,その後増大した状態が長く継続することが明らかになった。雌産仔では, 8週齢において接触逃避行動および対物攻撃行動が有意に増大したが,雄産仔に比較して顕著ではなかった。本研究の結果から,ダイオキシン胎盤・母乳経由暴露に起因する接触逃避行動および対物攻撃行動の発現時期は血漿アンドロゲン濃度が最高に達する時期にほぼ一致することが示された。本研究によって,TCDD胎盤・母乳経由摂取に起因する若年期行動異常発現は性ホルモン,特に男性ホルモン分泌の増加に影響されることを示唆する論拠が示された。, In utero and lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin(TCDD)is known to induce a variety of abnormal behaviors in juvenile animals. However, the precise timing of pubertal onset of these symptoms remains unclear, as does the presence of sex differences in manifestation of the symptoms. The present study evaluated touch response and aggressive biting behaviors to examine the hypothesis that pubertal increases in the secretion of sex hormones are related to the exhibition of abnormal behaviors induced by perinatal exposure to TCDD. Normal male and female ddY mice were housed together for mating, and female mice were administered 100 μg/kg of TCDD or an equivalent volume of vehicle (olive oil) by gavage on gestational days 7 and 14. Offspring were weaned on postnatal day 28 and group- housed. Kicking and biting responses were measured three times a week to evaluate touch escape and aggressive biting behaviors during postnatal weeks 5-12 using the Touch Response Meter (TRM). Most mice exhibited both kicking and biting behaviors intensely toward the stimulation sticks on the TRM Among male offspring, intensities of both responses were significantly increased at the end of postnatal week 7 or in postnatal week 8, with the increase continuing until the end of postnatal week 12. In female offspring, similar to male mice, both behaviors increased significantly, but the degree of change was smaller than that in male offspring. These findings indicate that onsets of touch escape and aggressive biting behaviors occur in postnatal week 7 or 8, and suggest that onsets of these abnormal behaviors are concurrent with the period of increased androgen secretion. Pubertal onset of the abnormal behaviors induced by perinatal exposure to TCDD may be related to increased secretion of sex hormones, particularly in male mice.

ダイオキシン類とはpolychlorinated dibenzo-p-dioxins（PCDDs），polychlorinated dibenzofurans（PCDFs），coplanar polychlorinated biphenyls（coplanar PCBs）の総称で，いずれも２つのベンゼン環が塩素で置換された類似した構造を持つ．塩素の位置と個数により多数の異性体が存在し，最も毒性が強い2,3,7,8-tetra-CDD（TCDD）の毒性を１とした場合の相対的な毒性（toxic equivalent factor）が約30 の異性体について決定されている．ダイオキシン類の急性毒性として，塩素痤瘡，肝障害，胸腺萎縮，脂質代謝異常，体重減少などが挙げられる．一方，ダイオキシン類は脂溶性で極めて安定した物質であり，生体内に長期にわたって残留するため，発癌性や次世代への影響，免疫系への影響などの慢性毒性が懸念されている．このようなダイオキシン類による慢性毒性はマウスなどの実験動物では報告されているが，ダイオキシン類に対する感受性は種差が極めて大きいこともあり，ヒトへの影響はほとんどわかっていない．ヒトに対するダイオキシン類の長期的な影響をうかがう唯一の手段は，1960 年代から1970 年代にかけて発生した大規模なダイオキシン中毒事件・事故である，（カネミ）油症，セベソ事件，台湾油症などの被害者を対象としたコホート研究であるといえる．油症は1968 年に福岡県，長崎県，広島県など西日本を中心に発生した，複数のダイオキシン類が混入した食用油による食中毒事件である．約2000 人の被害者が確認されており，現在でも被害者の血中ダイオキシン類濃度は健常人に比べて極めて高い（表１）．九州大学では油症発生以来，被害者の追跡調査を行っている．本稿ではダイオキシン類による免疫系への影響について，これまでに基礎研究で明らかにされた事項と油症患者の協力により得られたデータについて紹介する．

In 1968, the contamination of cooking oil by heat-degraded polychlorinated biphenyls (PCBs) caused a case of mass poisoning, the so-called Yusho incident. The cause of Yusho disease is thought to be ingested toxic substances, including not only PCBs but polychlorinated dibenzofuran (PCDFs) in Kanemi rice oil. Extensive studies have been performed since 1995 by the Yusho study group involving follow-up surveys of human blood concentrations of the casual compounds in Yusho patients as well as clinical trials of the acceleration of the excretion of these compounds in Yusho patients. We have previously measured dioxin concentrations in the blood of 649 Yusho patients in annual medical examinations from 2001 to 2009. We determined that the concentrations of 2,3,4,7, 8-PeCDF 1,2,3,4,7,8-HxCDF 1,2,3,6,7,8-HxCDF, and 3,3',4,4',5,5'-HxCB (#169) in the blood of Yusho patients were more than twice as high levels to as those of normal controls. In this study, we compared the concentrations of 2,3,4,7,8-PeCDF, 1,2,3,4,7,8-HxCDF, 1,2,3,6,7, 8-HxCDF, and 3,3',4,4',5,5'-HxCB (#169) in the blood of male Yusho patients with those of female Yusho patients. As a result, it was found that the mean concentrations of 2,3,4,7,8-PeCDF 1,2,3,4, 7,8-HxCDF 1,2,3,6,7,8-HxCDF, and 3,3',4,4',5,5'-HxCB (#169) in female Yusho patients were 2.9, 3.7, 2.4, and 1.3 times higher, respectively, than those of male Yusho patients.

The news about the attempted poisoning of Ukrainian presidential candidate Viktor Yushchenko with dioxin was given wide coverage in the world media. Abraham Brouwer, a professor of environmental toxicology at the Free University in Amsterdam, reported that Yushchenko was poisoned with pure TCDD, the most harmful known form of dioxin. His blood contained 100,000 units (pg/g of lipid) of the poison, the second highest concentration ever recorded. Physicians at the Vienna Clinic in Vienna, said that Yushchenko's face was disfigured but he will recover over time. The author attempted to calculate the amount of dioxin with which Yushchenko was poisoned, taking into consideration his toxic intake from the viewpoint of the Yusho investigation previously reported in Japan. Yushchenko's toxic intake was calculated at 1.89mg-TEQ. This value fairly agrees with the maximum incubative amount that exhibits toxic symptoms, mainly chlor-acne (a type of skin disease). This value is equivalent to a daily intake of dioxin over a period of 30, 000 years.

「ダイオキシン法」制定の起爆剤ともなったテレビ朝日「ニュースステーション」の特集を巡る「ダイオキシン訴訟」について検証した。この訴訟は、特集番組によって野菜栽培農家の名誉が傷つけられ野菜価格が暴落したとして所沢の農家376名がテレビ朝日と野菜のダイオキシン濃度を公表した株式会社環境総合研究所の所長を告訴したものである。 ところが、この放送で公表された野菜の分析最高値とされたものは、野菜ではなく加工食品の煎茶であった。そのためこの報道に不適切な点があったとして郵政大臣がテレビ朝日に注意勧告を行った。ところが、裁判ではある資料が証拠として採用され、一・二審は農家側の敗訴となった。証拠資料とは、摂南大学の宮田研究室が分析したという「所沢産白菜の分析結果」である。一・二審の裁判官は、この分析値が特集番組で公表された最高値に近似していたことから、報道内容は真実であると審判した。 ところが、三審の最高裁は「視聴者は、ほうれん草をメインとする所沢産の葉っぱ物に煎茶が含まれるとは通常考えない」、また証拠資料として採用された白菜については「氏素性の定かでない、わずか一検体の白菜の分析結果をもってそれが真実であるとした原審は、明らかな法令の違反がある」として、本件を原審に差し戻す判決を行った。農家側の実質的逆転勝訴となった。 最高裁は宮田研究室が提出した証拠資料に対して重大な疑念を表明した訳である。しかし、審理は専ら証拠資料の氏素性に集中したが、この特集番組の構成そのものにも審理を尽くすべき点があった。ここでは、なぜ、一・二審と三審で180度異なった判決が下されたのか、その背景も含めてこの裁判の問題点を明らかにした。

Sedimentation of Lake Suwa is much affected by flood sediments even in the center of the lake. The concentrations of dioxins and PAHs are diluted by such event sediment composed mainly of inorganic,non-contaminated materials. Flood sediment layers dated on 10 June 1950, 29 June 1961 and 28 September 1983 are confirmed in the cored sediments from Lake Suwa. Although the persistent organic pollutants are low in the flood sediments compared with the normal sediments below and above, the total amount of pollutants deposited in one flood is much larger than the annual amount of normal sediments. The annual changes of the persistent organic pollutants amount in the normal sediments well correspond with the history of human activities around the lake. Chemical and other analyses must be based sedimentary unit identified by lithology and density., Article, 第14回環境地質学シンポジウム論文集 : 323-328(2004)

近年の急速な技術革新や社会経済構造の変化に伴い、都市廃棄物の処理・処分問題は、廃棄物排出量の激増、質の複雑・多様化による処理困難物の増加、アメニティ環境に対する地域社会の関心の高まりなどによって構造的に変化しつつある。このような状況および地球環境保全、資源保全の観点から、本研究では都市廃棄物の適性処理・処分のみならず、資源化・再利用を含めたシステムの確立をはかることを最終目的としている。都市廃棄物の処理は、日本の国土が狭く人口密度が高いことから、都市ごみの80%近くが焼却処理されている。とくに大都市圏においては、狭く限られた地域において膨大な生産と消費が行われており、これに伴って発生するごみの焼却処理はさらに増加する傾向にあって、全量焼却も計画される現状にある。このように、都市廃棄物の処理・処分方法として現在だけでなく、将来にわたっても主流となると考えられる焼却処理に関しては、(a)安定燃焼技術、(b)排ガス・飛灰中の有害成分の防除法、(c)焼却残さの処理・処分、資源化・再利用技術、などについての検討が必要である。本研究ではこの中で都市ごみ焼却灰の適性処理・処分、資源化・再利用に関する国内外の技術、研究開発、実用化の現状について考察した。, The changes in social and economical structures and the innovation of technologies increases total amount of the municipal solid waste (MSW), and have brought changes in the MSW treatment in recent years. It is important to establish the proper waste disposal system and the recycling system from a stand point of the environment and the resource preservations. In Japan where land is limited and many people are concentrated in metropolitan areas, up to 80% of the MSW is incinerated. Especially, an enormous amount of production and consumption is made in the metropolitan areas. Therefore, the MSW incineration tends to increase with increasing the production. This concern has generated 100% MSW incineration plan. Thus, the incineration treatment will remain the main treatment of the MSW in future. Then, the research works for (a) a stabilized incineration technology. (b) a reduction technology in harmful ingredients, and (c) MSW incinerator ash disposal and waste and recycling technologies are urged. This report describes the present situation and the technical legislative trends for the proper MSW incinerator ash disposal and waste recycling technologies.